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90 publications mentioning hsa-mir-28

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-28. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 479
Other miRNAs from this paper: hsa-mir-100, hsa-mir-139, hsa-mir-518b
Western blotting showed that RAP1B expression in the xenograft tumors was slightly suppressed by overexpression of miR-28-5p (P = 0.095, Figure 8D–8E), while significantly increased by overexpression of RAP1B (P < 0.01, Figure 8D–8E) as compared with the control mice, and this suppression was mediated primarily through the suppression of the translation of RAP1B (Figure 8D–8E). [score:14]
To further examine miR-28-5p can inhibit RAP1B expression in vitro, we also stably overexpressed miR-28-5p by transfecting a lentiviral expressing vector of miR-28-5p into the above two cell lines. [score:9]
Transfection of miR-28-5p mimics inhibited RAP1B protein expression in renal carcinoma cells, and transfection of miR-28-5p inhibitor promoted RAP1B protein expression. [score:9]
A498 and ACHN cells were seeded in 96-well culture plates at 1 × 10 [4] cells/well (A498) or 2 × 10 [4] cells/well (ACHN), transfected with the indicated miR-28-5p mimics, miR-28-5p inhibitor, plenti-miR-28-5p, RAP1B vector, RAP1B siRNA or negative controls, and incubated for 12, 24, 48 and 72 h. Cell cycle analysis was conducted using flow cytometry after overexpressing or inhibiting miR-28-5p expression through transient transfection following 48 h culture. [score:9]
Figure 3(A– D) By western blotting analysis, RAP1B protein was significantly downregulated in A498 and ACHN cells transfected with miR-28-5p mimics or plenti-miR-28-5p and was upregulated with miR-28-5p inhibitor treatment. [score:9]
A498 cells were either infected with a lentiviral expression vector to express miR-28-5p or transfected with an RAP1B overexpression plasmid. [score:7]
A western blotting analysis showed that miR-28-5p overexpression in A498 cells not only suppressed the expression of RAP1B but also decreased the phosphorylation levels of p38 and Erk1/2. [score:7]
To further validate RAP1B as a legitimate target of miR-28-5p, we analyzed the expression of the endogenous RAP1B after transiently transfecting cells with miR-28-5p mimics or miR-28-5p inhibitor. [score:7]
miR-28-5p mimics and its negative control (NC) mimics-scramble, miR-28-5p inhibitor and its NC inhibitor-scramble, and the miR-28-5p mutant were obtained from GenePharma (Shanghai, China), and lentivirus to overexpress miR-28-5p was purchased from Invitrogen. [score:7]
miR-28-5p inhibits the tumorigenesis of RCC by directly downregulating RAP1B and influencing the activation of two MAP kinases in the MAPK signaling pathway, p38 and Erk1/2. [score:7]
Thus, we tested whether the suppression of the expression of RAP1B resulted by miR-28-5p overexpression affects the activation of these two MAP kinases in renal carcinoma cells. [score:7]
Our investigation of the downstream effects of the miR-28-5p/RAP1B signaling axis showed that miR-28-5p may inhibit the phosphorylation of MAPK signaling molecules by p38 and Erk1/2 through the downregulation of RAP1B expression. [score:6]
In contrast, RAP1B mRNA expression was not affected by overexpression or knockdown of miR-28-5p in A498 or ACHN cells (Figure 3E and 3F). [score:6]
Girardot et al. observed miR-28 overexpression in the platelets of patients with BCR-ABL negative myeloproliferative neoplasms, and they identified MPL, an important regulator for megakaryocyte differentiation, to be the main target of miR-28 [33]. [score:6]
As shown in the Figure 3H, as comparing with controls, expression of miR-28-5p mimics significantly suppressed the luciferase activity of the reporter, but had minimal effect on the mutant reporter, suggesting that miR-28-5p can bind directly to the RAP1B 3′-UTR. [score:6]
In contrast, knockdown of miR-28-5p with miR-28-5p inhibitor increased the expression of RAP1B and, at the same time, promoted the phosphorylation of p38 and Erk1/2; however, the total levels of p38 and Erk1/2 remained unchanged (Figure 7F and 7G). [score:6]
To explore the molecular mechanisms by which miR-28-5p affects RCC development, we predicted miR-28-5p target genes in RCC using the TargetScan [30], miRanda [31] and PicTar databases [32]. [score:6]
These results indicate that re -expression of RAP1B significantly rescue the miR-28-5p -mediated inhibition of cell growth and migration, and the miR-28-5p/RAP1B signaling axis has an important role in the development and progression of RCC. [score:6]
miR-28-5p expression is downregulated in RCC tissues and renal carcinoma cell lines. [score:6]
Gain-of-function and loss-of-function studies demonstrated that miR-28-5p acted as a tumor suppressor in RCC for multiple antitumor effects by directly inhibiting RAP1B. [score:6]
To understand the biological effect of miR-28-5p downregulation on the proliferation and migration of renal carcinoma cells, miR-28-5p expression was manipulated in vitro and gain-of-function and loss-of-function analyses were performed. [score:6]
By observing cell numbers passing through the matrigel membrane, we found that ectopic expression of miR-28-5p could significantly inhibit cell invasion ability in A498 and ACHN cell lines compared with controls, while transfection of miR-28-5p inhibitor significantly increase the invading cell population. [score:6]
An in silico search using three miRNA target databases identified seven genes as potential miR-28-5p targets. [score:5]
Moreover, re -expression of RAP1B significantly enhanced the wound-healing rate of A498 cells inhibited by miR-28-5p mimics (Figure 7E). [score:5]
Almeida MI et al. found that overexpression of miR-28-5p reduced CRC cell proliferation, migration and invasion in vitro and inhibited tumor growth in vivo [18]. [score:5]
Figure 6(A) Ectopic expression of miR-28-5p inhibited the invasion of A498 and ACHN cells in vitro. [score:5]
After 4 days of acclimatization, a total of 7 × 10 [6] A498 cells stably transfected with either the miR-28-5p overexpression lentiviral vector, RAP1B overexpression vector or control were injected subcutaneously into the right inside of the groin of each mouse (4 mice per group). [score:5]
miR-28-5p decreases the growth rate of renal carcinoma in vivoBecause our in vitro experiments revealed that miR-28-5p or RAP1B expression was associated with proliferative traits, we next examined the effect of miR-28-5p or RAP1B expression on tumor formation in vivo. [score:5]
Because our in vitro experiments revealed that miR-28-5p or RAP1B expression was associated with proliferative traits, we next examined the effect of miR-28-5p or RAP1B expression on tumor formation in vivo. [score:5]
In addition, overexpression of miR-28-5p significantly suppressed the colony formation, while the loss of miR-28-5p function obviously enhance the proliferation of RCC cell lines. [score:5]
Figure 1(A, B) qRT–PCR results showed downregulation of miR-28-5p expression in 33 primary RCC samples compared with matched adjacent non- tumorous samples. [score:5]
Their sequences were as follows: miR-28-5p mimics (sense) 5′-AAGGAGCUCACAGUCUAUUGAG-3′ and miR-28-5p mimics (anti-sense) 3′-C AAUAAGACUGUGAG CUCCUUU-5′; mimics-scramble (sense) 5′-UUCUCCG AACGUGUCACGUTT-3′ and mimic-scramble (anti-sense) 3′-ACGUGACACGUU CGGAGAATT-5′; miR-28-5p inhibitor (sense) 5′-CUCAAUAGACUGUAGCUCCU U-3′; inhibitor-scramble (sense) 5′-CAGUACUUU UGUGUAGUACAA-3′; RAP1B- siRNA1 (sense) 5′-GUGAGUAUAAGCUAGUCGUdTdT-3′; siRNA2 (sense) 5′-AC CUAGUGCGGCAAAUUAAdTdT-3′; and siRNA3 (sense) 5′-UGUUGGUAAUAU UGACdTdT-3′. [score:5]
The expression of miR-28-5p mimics significantly suppressed the luciferase activity of the wild type reporter but had minimal effect on the mutant reporter. [score:5]
As shown in Figure 7A and 7B, re -expression of RAP1B significantly reversed miR-28-5p-leaded inhibition of A498 and ACHN cell proliferation. [score:5]
Furthermore, in our cell based studies, re -expression of RAP1B almost completely reversed the miR-28-5p-imposed inhibition on proliferation and migration. [score:5]
To confirm the role of miR-28-5p/RAP1B axis in tumor cell proliferation or metastasis in vivo, we performed the immunohistochemistry analysis to assess the proliferative activity by using anti-Ki-67 and anti-PCNA monoclonal antibody in the tumors from mice implanted with control cells, miR-28-5p -overexpressing cells and RAP1B -overexpressing cells. [score:5]
In RCC tissues and renal carcinoma cells, miR-28-5p is expressed at a low level and RAP1B is expressed at a high level. [score:5]
To further clarify whether the tumor suppression roles of miR-28-5p were dependent on RAP1B expression, we performed a series of functional restoration assays in A498 and ACHN cells. [score:4]
Taken together, these results combined with the results of the in vitro assays, which confirmed the tumor suppressor role of miR-28-5p in renal carcinoma tumorigenesis through the targeting of RAP1B. [score:4]
To further confirm the role of miR-28-5p in renal carcinoma cell proliferation, we subsequently performed cell cycle analysis and colony formation assay when miR-28-5p was overexpressed or inhibited in A498 and ACHN cells, respectively. [score:4]
In another study, miR-28-5p was defined as a critical regulator of Mad2 translation and the function of the mitotic checkpoint in VHL -associated cancers [34]. [score:4]
Upregulation of RAP1B protein in RCC tissues and renal carcinoma cell lines is inversely correlated with miR-28-5p. [score:4]
In contrast, miR-28-5p inhibitor -mediated knockdown of miR-28-5p markedly enhanced renal carcinoma cell migration (Figure 5A and 5C). [score:4]
We performed a tumor formation assay in a nude mouse mo del using A498 cells stably expressing miR-28-5p after lentiviral infection or transfected with a RAP1B plasmid to overexpress RAP1B, and then cells were implanted subcutaneously into mice (Figure 8A). [score:4]
RAP1B is experimentally demonstrated as a direct target of miR-28-5p in renal carcinoma cells. [score:4]
Downregulation of miR-28-5p in RCC tissues and renal carcinoma cell lines. [score:4]
As shown in the Supplementary Figure S3, compared with the controls, A498 and ACHN cells transfected with miR-28-5p had a slightly higher percentage of cells in G1 phase and a lower percentage of cells in S phase, while inhibited miR-28-5p expressions had opposite effects, suggesting that miR-28-5p causes G1 arrest. [score:4]
Among these candidates, RAP1B, an oncogene previously shown to play critical roles in the regulation of cell proliferation and invasion [19– 25], was predicted to be a potential target of miR-28-5p (Figure 2A). [score:4]
Figure 7(A, B) CCK-8 assay indicated that the re -expression of RAP1B significantly reversed miR-28-5p -mediated inhibition of both A498 and ACHN cell growth. [score:4]
To examine whether miR-28-5p was dysregulated in RCC, we first determined the expression patterns of miR-28-5p in 33 RCC tissue samples and 33 corresponding adjacent non-tumorous tissues from the same patients using real-time quantitative reverse transcriptase PCR (qRT-PCR). [score:4]
Further studies should be performed to determine whether other targets of miR-28-5p and the signaling pathways they act on are involved in the mediation of RCC development and progression by miR-28-5p. [score:4]
miR-28-5p represses renal carcinoma cell proliferation and migration by directly targeting RAP1B. [score:4]
However, it is possible that other potential targets of miR-28-5p in addition to RAP1B may be involved in the regulation of renal carcinoma cell proliferation and migration. [score:4]
Validation of RAP1B as a direct target of miR-28-5p. [score:4]
To confirm whether RAP1B is a direct and specific target of miR-28-5p, we employed a luciferase reporter carrying the presumed site in the 3′-UTR of RAP1B mRNA. [score:4]
The data were analyzed using the ΔΔCt approach and expressed as the ration of miR-28-5p to U6 [2 [–ΔCt(miR-28-5p-U6)]]. [score:3]
The clinical information and the relative expression of miR-28-5p for these 20 paired tissue specimens were displayed in Supplementary Table S2. [score:3]
Thus, RAP1B was selected as a candidate target gene of miR-28-5p for further validation. [score:3]
Figure 5(A– D) Transwell migration assays using A498 and ACHN cells showed that miR-28-5p overexpression by transient transfection with miR-28-5p mimics or stable transfection with plenti-miR-28-5p both resulted in an increased number of relocated cells compared with vector control transfection, whereas miR-28-5p inhibitor -mediated knockdown of miR-28-5p markedly enhanced the migration of these cells compared with nontransfected counterparts. [score:3]
As shown in Figure 4A and 4B, overexpression of miR-28-5p by transient transfection of miR-28-5p mimics significantly reduced the growth rate of A498 and ACHN cells. [score:3]
These data reveal that miR-28-5p represses renal carcinoma cell proliferation and migration by targeting RAP1B, which we believe to be a novel function and mechanism of miR-28-5p and RAP1B in RCC. [score:3]
In addition, we also evaluated the expression level of RAP1B in xenograft tumors after ectopic overexpression of miR-28-5p or RAP1B. [score:3]
Stable ectopic expression of miR-28-5p in these cells was validated by qRT-PCR (Supplementary Figure S1C). [score:3]
The minimum free energy value of the hybridizations between miR-28-5p and RAP1B was −22.7 kcal/mol, which is well within the range of genuine miRNA-target pairs. [score:3]
As shown in Figure 8F, the cell proliferation rate, as measured by the ratio of Ki-67 and PCNA positive tumor cells, were increased in tumors from the RAP1B -overexpressing group and decreased in tumors from the miR-28-5p -overexpressing group (Figure 8F). [score:3]
miR-28-5p suppresses renal carcinoma cell proliferation. [score:3]
One predicted hybridization was observed between miR-28-5p and the 3′-UTR of RAP1B, with perfect base-pairing between the seed region and the cognate target (Figure 2B). [score:3]
Spearman's rank correlation analysis was used to examine the correlation between the relative expressions of miR-28-5p and RAP1B. [score:3]
This indicates that RAP1B is a bona fide target of miR-28-5p. [score:3]
These data suggest that miR-28-5p may involve in repressing the phosphorylation of p38 and Erk1/2 through the inhibition of RAP1B, and further demonstrating that RAP1B is a key mediator of miR-28-5p function. [score:3]
RAP1B was predicted to be a potential target gene of miR-28-5p by all three algorithms. [score:3]
Furthermore, the wound-healing assay showed that the rate of A498 cell wound-healing was drastically reduced by miR-28-5p overexpression (Figure 5E and 5F), and it was markedly increased by miR-28-5p inhibitor treatment compared with treatment with scramble counterparts (Figure 5E). [score:3]
cgi), to predict the potential target genes of miR-28-5p. [score:3]
The transient transfection efficiencies of miR-28-5p mimics and miR-28-5p inhibitor in renal carcinoma cell lines were detected by qRT-PCR (Supplementary Figure S2A and S2B). [score:3]
Luciferase reporter constructs containing regions of the RAP1B 3′-UTR with the indicated miR-28-5p target sites or mutant sites were cloned into a p-MIR-reporter plasmid (Ambion). [score:3]
miR-28-5p reduced approximately 30% of A498 and ACHN cell migration, and co -expression of the RAP1B vector restored cell migration to the baseline level (Figure 7C and 7D). [score:3]
Taken together, these results indicate that the miR-28-5p/RAP1B axis may provide further insight into the pathogenesis of RCC and may represent a potential novel therapeutic target for RCC. [score:3]
All three databases suggested that RAP1B is a miR-28-5p target gene, and we focused on this Ras-related GTPase for further study because it is an oncogene in a variety of tumors. [score:3]
A control construct was also generated in which the putative miR-28-5p target binding sequence was mutated (Figure 2B). [score:3]
miR-28-5p has been reported to be deceased in colorectal cancer (CRC) tissues and to inhibit colorectal cancer cell proliferation, migration and invasion in vitro [18]. [score:3]
Taken together, these results from clinical specimens and cell lines indicate that the expression of miR-28-5p is significantly deceased in renal cell carcinoma. [score:3]
RAP1B is a downstream target gene of miR-28-5p in RCC. [score:3]
The volume of xenograft tumor in the miR-28-5p-overexpression group was lower than in the negative control group. [score:3]
Similar results were found in these cell lines infected with the miR-28-5p overexpression lentivirus plenti-miR-28-5p as indicated in Figure 4C and 4D. [score:3]
However, there was no significant association between miR-28-5p expression in RCC tissues and gender, age, histological classification or tumor-node-metastasis (TNM) stage (data not shown). [score:3]
To elucidate the mechanisms through which miR-28-5p acts on RCC, we conducted an in silico search using three computational algorithms in combination, TargetScan [30] (Release 6.2, June 2012, http://www. [score:3]
Overexpression of plenti-miR-28-5p by a lentivirus did not affect RAP1B mRNA level in the above-mentioned cell lines either (Figure 3G). [score:3]
In this study, we focused on RAP1B and demonstrated that it was a functional target gene of miR-28-5p. [score:3]
As anticipated, RAP1B protein levels in both A498 and ACHN cells were dramatically reduced by miR-28-5p mimics and significantly increased by miR-28-5p inhibitor (Figure 3A and 3B). [score:3]
In contrast, silencing of miR-28-5p expression significantly promoted the growth of A498 and ACHN cells (Figure 4E and 4F). [score:3]
Through in vitro and in vivo miR-28-5p gain-of-function and loss-of-function studies, we further confirmed that miR-28-5p acted as a tumor suppressor in RCC. [score:3]
More importantly, we found an inverse correlation between RAP1B protein expression and miR-28-5p levels in RCC tissues. [score:3]
Effects of overexpression of miR-28-5p or RAP1B on the growth of renal cell carcinoma xenografts in mice. [score:3]
The present work was the first to show a significant decrease in miR-28-5p expression in RCC tumors, and this was true for the majority of samples tested. [score:3]
RAP1B is a candidate target gene of miR-28-5p. [score:3]
The secretion of RAP1B protein was also drastically diminished by the lentiviral miR-28-5p expression vector to the same degree as by miR-28-5p mimics (Figure 3C and 3D). [score:3]
A review of the existing literature shows that miR-28-5p is aberrantly expressed in several types of tumors and cancer cell lines; however, only a few studies have analyzed miR-28-5p function in cancer. [score:3]
Indicated plasmids and equal amounts (100 pmol) of miR-28-5p mimics, miR-28-5p inhibitor or NC RNA were transfected into the cells using Lipofectamine 2000 Reagent (Life Technologies). [score:3]
Figure 4(A– D) By CCK-8 assay, the proliferation of A498 and ACHN cells was significantly inhibited by transient transfection with miR-28-5p mimics or stable transfection with plenti-miR-28-5p. [score:2]
miR-28-5p expression was deceased in 20 of the 33 (60.6%) RCC tissues when compared to the matched non-tumorous tissues (P < 0.05, Figure 1A and 1B). [score:2]
Functional studies showed that RAP1B has an opposite effect to that of miR-28-5p in the regulation of renal carcinoma cell proliferation and migration in vitro and also has an opposite effect to that of miR-28-5p in xenograft tumor growth in vivo. [score:2]
Collectively, our data suggest that miR-28-5p strongly contributes to the development of renal carcinoma migration. [score:2]
Collectively, our data strongly suggest that RAP1B and miR-28-5p have opposing effects on the regulation of renal carcinoma cell migration. [score:2]
Compared with the control mice, ectopic overexpression of miR-28-5p decreased the tumor volume of the nude mice (P = 0.101, Figure 8B–8C). [score:2]
We then determined the miR-28-5p expression level in three human renal carcinoma cell lines, A498, ACHN and Caki1, and found that miR-28-5p was markedly deceased in all three cell lines compared with the immortalized primary human proximal tubular cell line HK-2 (Figure 1C). [score:2]
More importantly, there was a clear inverse correlation between RAP1B protein and miR-28-5p levels in the same 20 pairs of RCC tissues and corresponding noncancerous tissues (R = −0.573, P = 0.0083) (Figure 2E). [score:1]
The newly identified miR-28-5p/RAP1B axis provides further insight into the pathogenesis of RCC and opens new avenues for future RCC therapies. [score:1]
The miR-28-5p mutant was constructed by replacing the RAP1B binding site with its complimentary sequence. [score:1]
In this study, we explored the relationship between miR-28-5p and RCC and the potential mechanisms of miR-28-5p in RCC. [score:1]
However, contradictory roles for miR-28 have been reported in CRC. [score:1]
We found that miR-28-5p was decreased in RCC tissues. [score:1]
We next asked whether RAP1B was inversely correlated with miR-28-5p in human RCC tissues. [score:1]
Therefore, these in vitro results further confirmed that miR-28-5p had a biological effect on proliferation (Supplementary Figure S3). [score:1]
In combination with our previous results, our current findings suggest that miR-28-5p has an antitumorigenic role in RCC and, therefore, has potential as a novel biomarker and therapeutic agent for RCC. [score:1]
Based on our results, we propose the following mo del for the miR-28-5p/RAP1B signaling axis in RCC progression (Figure 8G). [score:1]
Computational analyses identified seven candidate genes containing potential miR-28-5p binding sites (Figure 2A). [score:1]
We first examined the expression levels of RAP1B in 20 paired randomly selected RCC tissues and adjacent non-tumorous tissues from the 33 paired tissue samples that were used for miR-28-5p measurement by immunohistochemistry (IHC) analysis. [score:1]
miR-28-5p represses renal carcinoma cell migration. [score:1]
However, the functional role and mechanism of action of miR-28-5p in RCC have not been elucidated. [score:1]
miR-28-5p represses the phosphorylation MAPK signaling molecules by p38 and Erk1/2. [score:1]
A498 cells with increased miR-28-5p or RAP1B levels were then implanted subcutaneously into 4-week-old C57/BL6 mice. [score:1]
We then examined the effect of miR-28-5p on tumor cell invasion. [score:1]
Furthermore, the miR-28-5p binding sequence in the RAP1B 3′-UTR was highly conserved across species (Figure 2B). [score:1]
These results demonstrated that miR-28-5p could attenuate cell invasion ability in renal carcinoma cells. [score:1]
miR-28-5p decreases the growth rate of renal carcinoma in vivo. [score:1]
These data suggest complex roles for miR-28-5p in multiple types of tumors. [score:1]
Taken together, these results demonstrated that miR-28-5p modulated the protein level, but not the mRNA level of RAP1B. [score:1]
A transwell migration assay using A498 and ACHN cell lines showed that ectopic expression of miR-28-5p using a transient transfection strategy with miR-28-5p mimics or a stable lentiviral infection strategy with plenti-miR-28-5p decreased the number of invaded cells compared with that of the corresponding controls (Figure 5A–5D). [score:1]
miR-28-5p attenuated cell invasion ability in A498 and ACHN cells (Figure 6A). [score:1]
For cell invasion assay, RCC cells (5 × 10 [4]) were transfected with miR-28-5p mimics, miR-28-5p inhibitor or negative controls, and cell invasion was performed by matrigel invasion assay. [score:1]
miR-28-5p represses renal carcinoma cell invasion and RAP1B promotes renal carcinoma cell proliferation and migration. [score:1]
Our previous study found that miR-28-5p was markedly decreased in sera from patients with RCC compared with that from normal controls, suggesting that miR-28-5p may be involved in the development of RCC [17]. [score:1]
This suggests that miR-28-5p might be involved in the pathogenesis of RCC. [score:1]
Next, we assessed the possible role of miR-28-5p in renal carcinoma cell migration. [score:1]
The recombinant wild type RAP1B 3′-UTR constructs or mutant 3′-UTR constructs were transfected into human renal carcinoma cell lines A498 and ACHN together with miR-28-5p mimics or negative controls. [score:1]
The expression level of miR-28-5p was measured using qRT–PCR and normalized against an endogenous control (U6 sRNA). [score:1]
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2
[+] score: 43
Other miRNAs from this paper: hsa-mir-17
These data indicate that upregulation of miR28-5p in peroxide -treated cells cultured in high glucose results in inhibition of sirtuin 3 expression. [score:8]
To determine if miR28-5p inhibits sirtuin 3 expression, we transfected peroxide -treated cells cultured in high glucose with a miR28-5p inhibitor. [score:7]
[29] We found that peroxide treatment under high-glucose conditions resulted in miR28-5p -mediated inhibition of sirtuin 3, identifying sirtuin 3 as a novel target of this miRNA. [score:5]
To confirm if sirtuin 3 is a direct target of miR28-5p, we simultaneously transfected cells with the miR28-5p mimic and a reporter plasmid in which the 3′ UTR sequence of sirtuin 3 had been inserted downstream of the secreted Gaussia luciferase (GLuc) reporter gene driven by a SV40 promoter. [score:4]
Sirtuin 3 is a direct target of miR28-5p. [score:4]
Recently, nuclear factor (erythroid-derived 2)-like 2, an oxidative stress -induced transcription factor involved in antioxidant defence, [40] was also identified as a target of miR28. [score:3]
Mimic and inhibitors for miR17-5p and miR28-5p as well as the respective controls were purchased from Life Technologies. [score:3]
[41] Increased miR28 expression by oxidative stress under high glucose conditions may therefore have far-reaching consequences leading to impaired antioxidant defence as well as activation of proapoptotic pathways. [score:3]
Interestingly, levels of miR28-5p were markedly higher in untreated controls cultured in high compared with low glucose, suggesting that extracellular glucose levels may regulate miR28-5p expression (Figure 5g). [score:3]
To determine the mechanism responsible for the reduction in sirtuin 3 levels in peroxide -treated cells in high glucose, we performed a database search of miRNAs predicted to target sirtuin 3. We found that the levels of one candidate miRNA, miR28-5p, were significantly higher in peroxide -treated cells cultured in high but not low glucose compared with untreated controls (Figure 5f). [score:2]
HmiT006079-MT05) GLuc-SEAP vector (GeneCopoeia, Rockville, MD, USA) with 30 nM of either miR28-5p mimic or mimic control using lipofectamine 2000 (all from Life Technologies). [score:1]
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3
[+] score: 37
A notable down-regulated mRNA target of miR-28 was PARL, a critical regulator of mitochondrial morphology and function. [score:7]
Another down-regulated mRNA target of miR-28 was BCCIP, a cofactor for BRCA2, which functions as a progesterone-responsive gene involved in DNA repair and cell cycle control [57]. [score:6]
Specifically, Let-7b and miR -28 have been shown to inhibit progesterone and testosterone production in human granulosa cells (GC), while miR-26a and miR-28 suppress estrogen secretion [44– 46]. [score:5]
In addition to inhibition of sex steroid production in vitro by both of these miRNA [45], miR-28 is over expressed during the E2 drop following dominant follicle selection [53]. [score:5]
regulated kinase 1A) 2.0 PPP1R16A (protein phosphatase 1, regulatory subunit 16A) 2.0Among the miRNAs that have been individually shown to be important for both CL function and adiposity, changes in miR-26 and miR-28 were notable. [score:3]
Published reports suggest that let7b, miR-26a and miR-28 inhibit sex steroid secretion from GC, while let7b, miR-26a, miR-28 and miR-143 decrease GC proliferation and let7b and miR-26a promote GC apoptosis [46]. [score:3]
regulated kinase 1A) 2.0 PPP1R16A (protein phosphatase 1, regulatory subunit 16A) 2.0 Among the miRNAs that have been individually shown to be important for both CL function and adiposity, changes in miR-26 and miR-28 were notable. [score:3]
Similarly, expression of let-7b, miR-26a, miR-28 and miR-143 were previously associated with decreased proliferation of GC, while let7b and miR-26a were found to promote GC apoptosis[45– 47]. [score:3]
Fformyltransferase) -4.6 B4GALT4 (UDP-Gal:betaGlcNAc beta 1,4- GST, polypeptide 4 -3.4 MCUR1 (mitochondrial calcium uniporter regulator 1) -3.0 PDCD10 (programmed cell death 10) -2.8 SRP19 (signal recognition particle 19kDa) -2.6 hsa-miR-28-3p (4,831) BCCIP (BRCA2 and CDKN1A interacting prtein) protein -4.9 PARL (presenilin associated, rhomboid-like) -4.8 hsa-miR-486-5p (-25,555) PTEN (phosphatase and tensin homolog) 6.0 FLRT2 (fibronectin leucine rich transmembrane protein 2) 5.0 ARHGAP5 (Rho GTPase activating protein 5) 4.0 ZNF701 (zinc finger protein 701) 4.0 GRAP (GRB2-related adaptor protein) 3.0 TEK (TEK tyrosine kinase, endothelial) 3.0 TTC31 (tetratricopeptide repeat domain 31) 3.0 VPS37B (vacuolar protein sorting 37 homolog B) 3.0 DYRK1A (dual-specificity TYR-(Y)-phos. [score:2]
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4
[+] score: 34
Among the 18 upregulated expression of miRNAs, 4 miRNAs including miR-15a, miR-16-2, miR-28 and miR-660 were validated in a large cohort of patients. [score:6]
Among these miRs, up-regulation of miR-16, miR-15a, miR-28 and miR-660 were also seen significantly changes in high HIP1 expressers in a large and independent cohort of TCGA patients (Fig. 3). [score:6]
For example, CCND3 gene regulated by miR-28-5p involved in P53 pathway, Wnt signaling pathway, cell cycle and Jak-STAT signaling pathway (Table S7), several targeted genes (ZYX, VCL, PDPK1, MAPK9, COL1A1, Tables S8 and 9) of miR-15/16 were involved in adhesion or migration processes; LFNG in notch signaling pathway was regulated by miR-660 (Table S10), etc. [score:5]
Specifically, among these 1137 aberrantly expressed genes, 84 genes were predicted to be targeted by miR-28-5p, 100 by miR-15a, 100 by miR-16 and 58 by miR-600 (Figure S6–9). [score:5]
Importantly, HIP1 interference in THP-1 cell line dramatically reduced the expression of miR-16, miR-15a, miR-28 and miR-660 (Fig. 5A). [score:3]
In addition, increased miR-28 expression leads to autonomous growth of hematopoietic cells by constitutive activation of STAT5 20. [score:3]
By means of miRNA-mRNA integrative analysis, we found several targeted genes of miR-28-5p, miR-15a, miR-16 and miR-660. [score:3]
In the KEGG analysis, these targeted genes of miR-28-5p, miR-15a and miR-16, miR-660 respectively involved in 77, 70, 83 and 33 different metabolic networks with oncogenic potential (Table S7–10). [score:3]
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5
[+] score: 20
In-silico Prediction of Target miRNAs against Human Nrf2 and Experimental Validation of Nrf2 Downregulation by Forced Expression of miR144, miR153, miR27a and miR142-5pNrf2, an essential transcription factor for regulating both basal and inducible expression of diverse cytoprotective genes [26], [27] has been recently demonstrated to be regulated by miR144 and miR28 in non-neuronal mo dels [22], [23]. [score:12]
Nrf2, an essential transcription factor for regulating both basal and inducible expression of diverse cytoprotective genes [26], [27] has been recently demonstrated to be regulated by miR144 and miR28 in non-neuronal mo dels [22], [23]. [score:5]
Recently, Keap1 independent regulation of Nrf2 by miR28 has been reported in breast cancer cells [23]. [score:2]
So far, there are only few studies in non-neuronal mo dels that has validated Nrf2 silencing by miR144 [22], miR28 [23] and miR34a [24]. [score:1]
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6
[+] score: 20
The miRNAs expressed at the highest levels coincided with those reported by previous studies, and were similar to those expressed by NBC in our study, though several divergences emerged between CLL and NBC, such as the previously reported overexpression of miR-150-5p, miR-29a-3p, miR-155-5p, or miR-101-3p, underexpression of miR-181a-5p, or miR-181b-5p [14– 19], and others not firmly established yet, including the highly divergent miR-451a, miR-28-5p, miR-144-5p, miR-486-5p, or miR-486-3p, within the overexpressed, and miR-126-3p, miR-365a-3p, miR-199a-3p, or miR-582-5p, within the underexpressed. [score:13]
However, 41 miRNAs were differentially expressed between CLL and NBC according to the Student t test (cut-off 2-fold, p<0.05), being 29 overexpressed in CLL, including miR-150-5p, miR-29a-3p, miR-29b-3p, let-7a-5p, miR-26a-5p, miR-451a, miR-155-5p, miR-101-3p, miR-28-5p, miR-144-5p, miR-486-5p, or miR-486-3p, and 12 underexpressed, including miR-181a-5p, miR-222-3p, miR-126-3p, miR-365a-3p, miR-181b-5p, miR-199a-3p, or miR-582-5p (Table 1). [score:7]
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7
[+] score: 18
While it cannot be totally excluded that the age-related or age-limited changes are due to disease status per se, the changes in the expression of these miRNAs with age seem not to be simply due to the disease status for the following two considerations: (a) the heat maps of the differentially expressed miRNAs (Figs 2 and 3) show that the age effect is much stronger than disease effect; and (b) in view of the direction of gene expression changes, except miR-652, miR-28-5p, miR-133b, and miR-7, the age effect on the expressions of other 12 disease-related miRNAs would be under-estimated rather than over-estimated. [score:18]
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8
[+] score: 18
The miR-28-3p was shown to target and prevent the translation of HTLV-1 RNA [217], whereas miR-28-5p, reported to target the HIV-1 RNA, has no binding site on HTLV-1. Interestingly, the ATK-1 strain of HTLV-1 harbors a single-nucleotide polymorphism within the miR-28-3p binding site, and, thus, is resistant to the miR-28-3p. [score:7]
Compared to the activated CD4 [+] T-cells, resting memory CD4 [+] T-cells displayed upregulation of five miRNAs—miR-28, miR-125b, miR-150, miR-223, and miR-382, which negatively targeted the 3′-ends of HIV-1 mRNAs [179]. [score:5]
Wang et al. [223] reported that monocytes expressed elevated levels of the cellular miRNAs miR-125b-5p, miR-28-5p, miR-150-5p, miR-223-3p, and miR-382-5p, all previously shown by Huang et al. [179] to impair HIV-1 replication in resting CD4 [+] T-cells. [score:3]
Bai X. T. Nicot C. miR-28-3p is a cellular restriction factor that inhibits human T cell leukemia virus, type 1 (HTLV-1) replication and virus infectionJ. [score:3]
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9
[+] score: 18
Amongst the 13 miRNAs we selected, 6 miRNAs (miR-28-5p, miR-125b-5p, miR-150-5p, miR-155-5p, miR-223-3p, and miR-92a-3p) show up-regulated expression and 3 miRNAs (miR-29a-3p, miR-29b-3p, and miR-133b) show down-regulation of expression in patient samples, compared to uninfected counterparts. [score:10]
An interesting finding by Huang et al. suggested that a cluster of miRNAs (miR-28-5p, miR-125b-5p, miR-150-5p, miR-223-3p and miR-382-5p) have enriched expression in resting primary CD4+ T lymphocytes and have direct target sites on HIV-1 mRNA, thus leading to differential HIV-1 infectivity/resistance to different cells lying at varying developmental stages 11. [score:7]
In our study, there are 6 miRNAs (miR-28-5p, miR-125b-5p, miR-150-5p, miR-155-5p, miR-223-3p and miR-92a-3p) that are up regulated in patients (compared to uninfected controls). [score:1]
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10
[+] score: 16
Multiple post-transcriptional regulations can also be found in Figure  3. For example, 'hsa-miR-191’ is identified to suppress gene 'REPS1’ (RALBP1 associated Eps domain containing 1) in Figure  3(A), and 'hsa-miR-28-5p’ to suppress gene 'CIT’ (rho-interacting, serine/threonine kinase 21) in Figure  3(B). [score:6]
A better understanding of the activated regulation among 'hsa-miR-28-5p’, 'BRCA1’ and 'TUBB’ could be important to designing the miRNA gene therapeutic trials targeting IAV host factors [21]. [score:4]
As an example of co-regulations, the 'hsa-miR-28-5p’-'BRCA1’-'TUBB’ regulation motif can be seen in Figure  3(B). [score:3]
This module contains the regulatory motifs 'BRCA1’-'has-miR-28-5p’-'TUBB’/'POLR2A’, “EGR1’-'hsa-miR-155*’, 'EGR1’-'hsa-miR-146a’-'LTB’ and 'BRCA1’-'hsa-miR-146a’-'PHF1’. [score:2]
, and the second motif cluster contains 'BRCA1’-'hsa-miR-28-5p’-'TUBB’/'POLR2A’. [score:1]
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11
[+] score: 15
Sixteen of 359 miRNAs detected were differentially expressed between tumor and matched benign tissue (adjusted p < 0.05): 9 were upregulated (hsa-miR-19a; hsa-miR-512-3p; hsa-miR-27b; hsa-miR-20a; hsa-miR-28-3p; hsa-miR-200c; hsa-miR-151-3p; hsa-miR-223; hsa-miR-20b), and 7 downregulated (hsa-miR-22; hsa-miR-516-3p; hsa-miR-370; hsa-miR-139-5p; hsa-let-7e; hsa-miR-145-3p; hsa-miR-30c) in tumor tissue in comparison to matched benign tissue (Table 2). [score:9]
miRNA Expression Cancer association (Y/N) Upregulated (Y/N) hsa-miR-19a Common YY (10) hsa-miR-512-3p T and E only YN (11) hsa-miR-27b Common YY (12) and N (13) hsa-miR-20a Common YY (14) hsa-miR-28-3p Common YY (15) hsa-miR-200c Common YY (16) and N (17) hsa-miR-151-3p Common YY (18) hsa-miR-223 Common YY (19) and N (15) hsa-miR-20b Common YY (20) hsa-miR-22 T and E only YY (19, 21) and N (22) hsa-miR-516-3p T only N N/A hsa-miR-370 Common YY (23) hsa-miR-139-5p Common YN (24) hsa-let-7e Common YN (25) hsa-miR-145-3p T and E only YN (26) hsa-miR-30c Common YN (27) T, tumor; E, exosome. [score:6]
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12
[+] score: 14
High glucose coupled with oxidative stress results in the upregulation of miR-28-5p, which directly inhibits the expression of p53 deacetylase SIRT3 and leads to the increased level of acetylated p53 [87]. [score:9]
Meanwhile, the expression levels or activities of p53 and HIF-1 are also under the direct or indirect control of several microRNAs, such as miR-183, miR-28-5p, and miR-99a, through the acetylation and deacetylation modification. [score:5]
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13
[+] score: 14
This aneuploidy phenotype in VHL -deficient renal carcinoma cell lines is suppressed by ectopic expression of Mad2, a regulator of APC/C (85) or inhibition of miR-28-5p, a key regulator of Mad2 protein translation upregulated in a variety of cancers (84, 87). [score:14]
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14
[+] score: 14
miR miRNA-Cluster in vitro Glomeruli in Biopsy Selected Validated Targets miRPath KEGG Target Pathway Higher Lower Higher Lower let-7c-5p miR-99a C+ C− DSA+ TGFBR1, HMGA2, MPL Apoptosis, PI3K-Akt-Signalling, NF-kappa B Signalling, Cell Cycle, ErbB Signalling, TGF-beta Signalling miR-28-3p None C+ C− DSA+ None found. [score:5]
An in vitro study in cardiomyocytes describes suppression of the PDPK1/AKT1/MTOR signalling pathway as a function of miR-28-3p. [score:3]
Based on inspection of the volcano plots and an in silico analysis of regulated pathways with DIANA miRPath v. 2.0 [10] we chose a set of 16 miRNAs for confirmation in microdissected glomeruli from patients with only HLA-class I DSAs: miR-let-7c, miR-28-3p, miR-29b, miR-30d, miR-99b, miR-125a-5p, miR-133a, miR-138, miR-146b, miR-195, miR-374b-3p, miR-484, miR-501-3p, miR-520e, miR-625-3p, miR-885-5p (Table  1). [score:2]
Glomerular miR-let-7c-5p (a), miR-28-3p (b), miR-30d-5p (d), miR-99b-5p (e), miR-125a-5p (f) and miR-195-5p (j), miR-374b-3p (k), miR-484 (l), miR-501-3p (m), miR-520e (n) and miR-885-5p (p) were higher in DSA+ than to controls. [score:1]
Thus, less miR-28-3p in DSA+ could have proinflammatory effects. [score:1]
miR-28-3p was one of three miRNAs, which were lower in DSA+ than in controls. [score:1]
median 0.24; IQR 0.20; 0.43; p < 0.001), so were miR-28-3p (0.40; 0.24; 2.60 vs 0.19; 0.11; 0.27; p = 0.011), miR-30d-5p (0.57; 0.33; 0.81 vs. [score:1]
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15
[+] score: 12
0 hsa-mir-98 dbDEMC;miR2Disease hsa-mir-411 dbDEMC;HMDD v2.0 hsa-mir-28 dbDEMC hsa-mir-22 dbDEMC;miR2Disease;HMDD v2.0 In this study, we implemented both global and local LOOCV validation methods based on 5430 known miRNA-disease associations between 383 diseases and 495 miRNAs from HMDD v2.0 to evaluate the prediction accuracy of. [score:7]
0 hsa-mir-98 dbDEMC;miR2Disease hsa-mir-411 dbDEMC;HMDD v2.0 hsa-mir-28 dbDEMC hsa-mir-22 dbDEMC;miR2Disease;HMDD v2.0 The first column records top 1–25 related miRNAs. [score:5]
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16
[+] score: 11
017−3.45 (0.29)miR-210.017−4.35 (0.23) UpregulatedmiR-302c0.047−3.46 (0.29)miR-28–3p0.041−3.30 (0.30)miR-30d0.0012.14miR-90.016−3.39 (0.30) UpregulatedmiR-23a0.0144.32miR-30c0.012−3.80 (0.26)miR-18a0.0422.35miR-142–3p0.0214.36miR-320a0.034−5.42 (0.18)miR-142–3p0.0223.71miR-1430.03710. [score:7]
Based on statistical significance (p<0.05) and 2 -FC, curcumin pretreatment attenuated the H [2]O [2] -induced expression of 17 miRNAs (miR-15b, miR-17, miR-21, miR-26b, miR-27b, miR-28–3p, miR-30b, miR-30d, miR-92a, miR-125a-5p, miR-141, miR-196b,, miR-195, miR-302a, miR-302c, miR-320a, and miR-9), which were also significantly reduced by the curcumin treatment alone (Figure 4, Table 2). [score:3]
007−3.33 (0.30)Let-7d0.001−7.09 (0.14)miR-30a0.006−3.67 (0.27)miR-26b0.013−4.26 (0.24)let-7i0.036−9.51 (0.17)miR-30b0.029−2.72 (0.37)miR-170.023−4.06 (0.25)miR-106b0.04−7.22 (0.14)miR-423–3p0.04−6.15 (0.16)miR-15b0.037−7.94 (0.13)let-7g0.005−7.23 (0. 14)let-7i0.027−5.91 (0.17)miR-302a0.019−4.06 (0.25)miR-28–5p0.011−12.99 (0.08)miR-106b0.034−9.15 (0.11)miR-30c0.014−3.46 (0.29)miR-374a0.044−9.93 (0.10)miR-170.04−2.84 (0.35)miR-90.007−4.13 (0.24)miR-1000.007−10.4 (0.10)miR-15b0.034−10.18 (0.10)miR-196b0.032−3. [score:1]
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17
[+] score: 11
It is known that miRNA-28 and miRNA-125b can target the 3’UTR of HIV transcripts (49). [score:3]
miRNA-28 and miRNA-125b are known to target 3’UTR of HIV transcripts (66). [score:3]
In addition to the ISGs, Poly I:C-stimulated IECs expressed HIV restriction miRNAs (Figure 4), including miRNA-17, miRNA-20, miRNA-28, miRNA-29 family members (miR-29a, 29b, and 29c), and miRNA-125b. [score:3]
We also found that the anti-HIV miRNAs: miRNA-17, miRNA-20, miRNA-28, miRNA-29 family members (miR-29a, 29b, and 29c) and miRNA-125b were increased in the exosomes (Figure 4B) from Poly I:C-stimulated IECs. [score:1]
We also observed that exosomes from Poly I:C-stimulated IECs were enriched with antiviral cellular ISGs and miRNAs (Figure 4), including miRNA-17, miRNA-20, miRNA-28, miRNA-29 family members (miR-29a, 29b, and 29c) and miRNA-125b. [score:1]
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18
[+] score: 11
miR-125b is a member of anti-HIV-1 miRNA family (including miR-28, miR-125b, miR-150, miR-223, and miR-382) that targets the 3′UTR of HIV-1 transcripts and inhibit viral translation, a post entry step. [score:7]
Our microarray data revealed downregulation of an array of cellular miRNAs (data not shown) including anti-HIV-1 miRNAs (miR-125b, miR-150, miR-28-5p, miR-223, and miR-382) in cocaine treated cells (Fig. 3A). [score:4]
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19
[+] score: 10
In HIV infection, increased expression of miRNA-223, miRNA-382, miRNA-125b, and miRNA-28 targets the 3′ UTR of HIV-1 mRNA, which may subsequently decrease HIV replication. [score:5]
In HIV infection, miRNA-223, miRNA-382, miRNA-125b, and miRNA-28, targets the 3′ untranslated region (UTR) of the HIV-1 messenger RNA, while miRNA-150 binds to Nef 3′ long terminal repeats (LTR) at 773 and 89 positions (Huang et al., 2007). [score:5]
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20
[+] score: 10
Of these, 14 (miR-23b, miR-28, miR-98, miR-103, miR-107, miR-193a,0, miR-324-5p, miR-324-3p, miR-331, miR-374, miR-432, miR-502, and miR-660) were upregulated and 6 (miR-31, miR-451, miR-452, miR-565, miR-594 and miR-659) were downregulated. [score:7]
[26]↑ pMyo diff [33]↑ muscle development [31]↓ muscle development [32]10 miR-27b↑(this study)↑ pMyo [13, 33] ↑ C2C12 diff [28, 33]  11 miR-28 (n)↑(this study)-  12 miR-29a↓(this study)↓ C2C12 diff [28] ↑ C2C12 diff [33]  13 miR-30a-5p↑↑(this study)↑ C2C12 diff [28, 33]  14miR-30a-3p↑(this study)↑ C2C12 diff [33]  15↑↑pMyo diff. [score:3]
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21
[+] score: 10
We performed Monte Carlo analysis on the 2102Ep and NTera-2 differential gene expression datasets and cross-referencing with the results with the differential miRNA expression results revealed 10 miRNAs in 2102Ep cells (mir-26a, miR-28, miR-30c, miR-148a, miR-200b, miR-517b, miR-518a-3p, miR-518b, miR-518c, miR-518f) and two miRNAs in NTera-2 cells (miR-200c and miR-367) to be potential master regulators of their inversely regulated target genes. [score:9]
While miR-26a, miR-30c, miR-148a, miR-200b, miR-200c and miR-367 are broadly conserved across vertebrate species, miR-28 is conserved only in mammals and miR-517b, miR-518f, miR-518b, miR-518c, miR-518a-3p, all as members of the C19MC polycistron, are found only in primates. [score:1]
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[+] score: 10
In addition, the authors also found that SNHG1, SNORD28, and sno-miR-28 were all significantly upregulated in select breast tumors and that sno-miR-28 overexpression enhanced breast epithelial cell proliferation. [score:6]
The authors of this work go on to show that the most highly expressed of these sdRNAs, sno-miR-28, actively represses the p53-stabilizing gene (TAF9B), thereby creating a regulatory feedback loop charged with controlling p53 stability. [score:4]
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23
[+] score: 9
In gluteal tissue, hsa-miR-27b, hsa-miR-196b and hsa-miR-28-5p were found to be both associated with their target mRNAs, as well as being tissue differentially expressed. [score:5]
Seven of the miRNAs that were differentially expressed in both studies, have previously been reported to play a role in tissue development, obesity, T2D and metabolic disturbances (hsa-miR-34a [23], [32], hsa-miR-28-5p [32], hsa-miR-27b [13], [15], hsa-miR-326 [21], hsa-miR-204 [22], [23], hsa-miR-195 [32], hsa-miR-519d [29]). [score:4]
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24
[+] score: 9
For the detection of differentially expressed microRNAs we analyzed 240 target miRNAs with four different normalization methods: Recommendation of (i) geNormPlus (geometric mean of miR-26b-5p and miR-195-5p (Pool A) as well as of miR-720, miR-1274a, miR-1260a and miR-30a-5p (Pool B)), (ii) NormFinder (geometric mean of miR-28-5p, miR-127-3p and miR-181a-5p (Pool A) as well as miR-10b-3p, miR-181a-2-3p and miR-720 (Pool B)), (iii) global mean normalization method, (iv) two most stable snoRNAs (geometric mean of RNU44 and RNU48 (Pool A) as well as RNU48 and snRNU6 (Pool B)) or (v) geometric mean of all three snoRNAs provided by the manufacturer. [score:5]
In contrast, NormFinder identified miR-28-5p, miR-127-3p and miR-181a-5p for Pool A as well as miR-10b-3p, miR-181a-2-3p and miR-720 for Pool B as the most stable miRNAs (Fig. 2). [score:1]
Relative expression levels were calculated using the following normalization methods: geNormPlus (miR-26b, miR-195-5p) NormFinder (miR-28-5p, miR-127-3p, miR-181a-5p), global Mean, best two snRNAs (RNU44, RNU48) and all 3 snRNAs (RNU44, RNU48, snRNU6). [score:1]
In order to provide a set of reference miRNAs one could suggest the intersection of the best 15 reference genes from both algorithms geNormPlus and NormFinder (miR-10b-3p, miR-1260a, miR-127-3p, miR-1274a, miR-181a-5p, miR-181a-2-3p, miR-195-5p, miR-26b-5p, miR-28-5p, miR-30a-3p, miR-30a-5p, miR-30d-5p, miR-361-5p, miR-720, miR-92a-3p). [score:1]
Based on our analysis we suggest miR-26b-5p (best according to geNormPlus) and miR-28-5p (best according to NormFinder) and one snoRNA (RNU44) as suitable reference genes choice for human glomerular miRNA quantification in IgA nephropathy. [score:1]
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25
[+] score: 9
Other miRNAs from this paper: hsa-let-7b, hsa-mir-15a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-100, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-221, hsa-mir-1-2, hsa-mir-15b, hsa-mir-30b, hsa-mir-122, hsa-mir-132, hsa-mir-141, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-195, hsa-mir-200c, hsa-mir-1-1, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-371a, hsa-mir-372, hsa-mir-373, hsa-mir-375, hsa-mir-151a, hsa-mir-429, hsa-mir-449a, hsa-mir-483, hsa-mir-193b, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-449b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320b-2, hsa-mir-891a, hsa-mir-935, hsa-mir-1233-1, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-1275, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1973, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-1233-2, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Finally, hsa-miR-19b [47, 54] and hsa-miR-483-5p [47, 53], which are upregulated, and hsa-miR-28-5p [47, 53], hsa-miR-19a [48, 53] and hsa-miR-1973 [48, 51], which are downregulated, are expressed in spermatozoa, but they have not been associated with spermatogenesis or related processes. [score:9]
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26
[+] score: 8
In a ground-breaking study, Huang et al. showed that a selected group of miRNAs, including miR-28, miR-125b, miR-150, miR223, and miR-382, bound to the 3′ UTR of viral mRNAs and showed that activation of resting CD4+ T cells resulted in downregulation of these miRNAs, which correlated with enhanced HIV-1 susceptibility (181). [score:4]
For example, stimulation of TLR3 was shown to induce an anti-HIV effect in primary macrophages, partially through upregulation of miR-28, miR-125b, miR-150, and miR-382 (182). [score:4]
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27
[+] score: 7
Comparison of 5p and 3p expression among 50 top-ranked miRNAs found in primary human chondrocytes demonstrated that three miRNAs, miR-320a, miR-28 and miR-103a-2, showed expression of their 3p arm only and four miRNAs, miR-199b, miR-98, miR-186 and miR-16-1, expressed their 5p arm only. [score:7]
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28
[+] score: 7
However, only a small number of microRNAs, including miR-28, miR-93, miR-144, miR-153, miR-27a, miR-132, and miR142-5p, have been confirmed experimentally to directly bind to the 3′UTR of Nrf2 and consequently downregulate gene expression [104– 108]. [score:7]
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29
[+] score: 7
Interestingly, hsa-miR-28 is upregulated by IFN response revealing a mechanism where innate immune response helps viral persistence by reducing virus dissemination to neighboring cells, diminishing local inflammation, and enabling the survival of infected cells. [score:4]
miR-28-3p is a cellular restriction factor that inhibits human T cell leukemia virus, type 1 (HTLV-1) replication and virus infection. [score:3]
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In addition, the up-regulation of four anti-HIV-1 miR (miR-28, miR-125b, miR-150, miR-382) was reported in macrophages treated with both IFN-α and IFN-β, and was shown to partially contribute to inhibition of HIV-1 infection in these cells [116]. [score:6]
[111] ↑ miR-155; miR-7 IL4-DCs (Setting 3)IFN-α/ β TNF α/ PGE [2]/ IFN-α/βSTAT1STAT4[62] pDCs IFN-α↑ miR-155 miR-155 *[114] pDCs IFN-α/β ↑ miR-146a[115] IFN-DCs (Setting 1) IFN-α/ω IFN-βCXCL11FCGR, MARCO, CLEC5A, DEFB1, IDO1[32] MDMs IFN-α/β ↑ miR-28; miR-125b; miR-150; miR-382[116] IFN-DCs (Setting 1) IFN-α LOX-1[40] IL4-DCs (Setting 3) RSV/ IFN-β * ↑ miR Let7b[117] IFN-DCs (Setting 1) IFN-α TLR7[27] PBMCs Type I IFNs ↑ miR146a[118] IFN-DCs (Setting 1) IFN-α TRAIL, granzymes, KLRs and other NK cell receptors, DCLAMP, CCR7 and CD49d[26] PBMCs MS/ IFN-β ** ↓ mir-29 family[119] IFN-DCs (Setting 1) IFN-β IL-6, IL-1β, IL-10, CCL20, CCL3, CCL5, CXCR4, CCR5, CCR2,CD44, TLR2, TLR4, CLECSF12, PRG1, TAP1, β2 microglobulin, CD74, CD1a, CD68 LAMP-3, NFkB2, SOD2, Cdc42, IFIT1[31] PBMCs (healthy donors) IFN-α ↑ miR-1; miR-30; miR-128; miR-196; miR-296;[120] PBMCs (CHC) IFN-α ** ↑ miR-1; miR-30; miR-296; Notes: A summary of representative type I IFN modulated genes (left column) or miR (right column). [score:1]
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[+] score: 7
Expression stability of the reference miRNA combination (miR-28, miR-103, and miR-106a) and reference gene PPIA. [score:3]
The miRNA expression data were normalized to the reference gene combination of miR-28, miR-103, and miR-106a [18]. [score:3]
Normalization was assessed with the reference miRNA combination miR-28, miR-103, and miR-106a [18], (S2 Fig). [score:1]
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[+] score: 7
For example, the opioid system inhibits expression of anti-HIV miRNAs (e. g., miRNA-28, 125b, 150, and 382) that target 3′-UTR of HIV transcripts (Wang et al., 2011). [score:7]
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[+] score: 6
For example, miR-382, miR-198, miR-223, miR-125b, and miR-28 inhibit HIV replication by modulating host cellular factors or by directly targeting the HIV genome (10, 11). [score:6]
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[+] score: 6
Dysregulated miRNA expression and function contribute towards the pathogenesis of numerous hematologic diseases, including miR-29b in acute myeloid leukemia [7], miR-145 and miR-146a in the 5q- syndrome [8], [9], mir-125b-2 in acute megakaryoblastic leukemia [10], miR-28 in myeloproliferative neoplasms [11] and miR-155, miR-21 and miR-210 in B-cell lymphomas [12]. [score:6]
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[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-21, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-30a, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30d, hsa-mir-34a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-194-1, hsa-mir-194-2, hsa-mir-200a, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-196b, hsa-mir-484, hsa-mir-486-1, hsa-mir-1271, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-27a, bta-mir-30d, bta-mir-484, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-98, bta-mir-148b, bta-mir-200a, bta-mir-30a, bta-let-7a-1, bta-mir-342, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, bta-mir-99b, hsa-mir-885, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-143, bta-mir-152, bta-mir-16a, bta-mir-194-2, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-199a-2, bta-mir-26a-1, bta-mir-28, bta-mir-335, bta-mir-338, bta-mir-378-1, bta-mir-486, bta-mir-885, bta-mir-96, bta-mir-1271, bta-mir-2299, bta-mir-199c, bta-mir-1388, bta-mir-194-1, bta-mir-378-2, hsa-mir-378b, bta-mir-3431, hsa-mir-378c, hsa-mir-4286, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, bta-mir-4286-1, bta-mir-4286-2, hsa-mir-378j, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, bta-mir-378d, bta-mir-194b, bta-mir-194b-2
When compared with the control period (day-14), we identified a total of 22 DE miRNAs at day+28 including 10 up-regulated (bta-miR-199c, miR-199a-3p, miR-98, miR-378, miR-21-5p, miR-148b, miR-34a, miR-152, miR-16a, and miR-28) and 12 down-regulated (bta-miR-200a, miR-145, miR-99a-5p, miR-125b, miR-99b, miR-125a, miR-96, miR-484, miR-1388-5p, miR-342, miR-486 and miR-1271) (Table  2). [score:6]
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[+] score: 6
As shown in Table 1, expression of 13 miRNAs was > 2 times higher or lower than in controls (p < 0.05), including only two miRNAs (rno-let-7a and rno-miR-28) that were up-regulated. [score:6]
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[+] score: 6
For CRC, different degrees of correlation were found for the 24 miRNAs exhibiting altered expression: miR-106a was not correlated at all, while miR-195 exhibited the largest number of ties and was taken as a root node with 9 edges (degree 15.86); 8 links were detected for miR-28-3p (degree 15.66), and 7 links for miR-1280 (degree 13.79), miR-1246 (degree 13.05), and miR-140-3p (degree 12.12) (Figure 5, panel A). [score:3]
In CRC network, as shown in panel A, m iR-195, miR-28-3p, miR-1280, miR-18a and miR-1246 exhibit the highest weighted degree rank. [score:1]
php), except miR-31 and miR-28-3p, which belong to the EGF pathway. [score:1]
The latter 3 nodes were also interconnected with miR-28-3p, which showed a high betweenness value. [score:1]
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[+] score: 5
The highly expressed cellular miRNAs miR-125b, miR-150, miR-28, miR-223 and miR-382 repress HIV-1 replication by targeting nef 3′-long-terminal repeat (LTR) region and contribute to viral latency in resting CD4 [+] T lymphocytes [15]. [score:5]
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[+] score: 5
While miR-21, miR-30a and miR-373 were expressed in all 7 tissues including testis, kidney, lung, spleen, heart, liver and skeletal muscle, miR-422, miR-28, miR-379, miR-431 and miR-648 demonstrated more restricted expression patterns (Figure 2). [score:5]
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[+] score: 5
Recently, Huang et al. have shown that miR-28, -125b, -150, -223, and -382, cellular miRNAs that are overexpressed in quiescent T4 lymphocytes, target sequences in the 3′ end of HIV-1 RNA, silencing thus almost all viral messengers [31]. [score:5]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-148b, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The 3p arms of miR-28 and miR-339 showed higher expressions than the corresponding 5p arms in the metastatic line, whereas they showed lower expressions than the corresponding 5p arms in the non-metastatic line. [score:5]
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[+] score: 5
Similarly, a cluster of cellular miRNAs, including miR-28, miR-125b, miR-150, miR-223 and miR-382, target the 3′ ends of HIV-1 mRNAs in cultivated resting CD4 [+] T cells to affect HIV-1 latency, and potently inhibit HIV-1 production [7]. [score:5]
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[+] score: 4
miR-28-3p was selected due to its stable expression across all samples in the whole genome. [score:3]
RT-qPCR data analysis was performed in R. Two technical replicates per sample were averaged and normalized against house-keeping control TBP (for genes) or miR-28-3p (for miRNAs) to yield the ΔC [q] values [18]. [score:1]
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[+] score: 4
With the aid of IPA pathway designer, we found that 27 of the 31 down-regulated miRNAs were linked to one or more mRNA networks and 20 of them (let-7 g, miR-101, miR-126, miR-133a, miR-142-5p, miR-150, miR-15a, miR-26b, miR-28, miR-29b, miR-30a, miR-30b, miR-30c, miR-30d, miR-30e, miR-34b, miR-99a, mmu-miR-151, mmu-miR-342 and rno-miR-151) were involved in all of the top 4 networks. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-93, hsa-mir-100, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-34a, hsa-mir-181c, hsa-mir-182, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-217, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-134, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-106b, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-372, hsa-mir-382, hsa-mir-148b, hsa-mir-196b, hsa-mir-424, hsa-mir-448, hsa-mir-449a, hsa-mir-483, hsa-mir-491, hsa-mir-501, hsa-mir-503, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320c-1, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320c-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
The miRNAs that directly bind to the 3′UTR of HIV-1 RNA (Fig.   2) include miR-28, miR-125b, miR-150, miR-223 and miR-382, which are highly expressed in resting CD4+T cells [73]. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-17, hsa-mir-21, hsa-mir-93, hsa-mir-130b
Bai X. T. Nicot C. miR-28-3p is a cellular restriction factor that inhibits human T cell leukemia virus, type 1 (HTLV-1) replication and virus infection J. Biol. [score:3]
Recently, host restriction factors such as SAMHD1, APOBEC3 and miR-28-3p have been shown to limit HTLV-1 infection [35, 36, 37]. [score:1]
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[+] score: 4
Our analysis of the genome-wide effects of DAC on cellular miRNAs, implicated significant down-regulation of miR-28 in all three cell lines, miR-21 in both cancerous cell lines and miR-17 in the non-aggressive cell line (Table 2; Dataset S5). [score:4]
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[+] score: 4
In the main study plasma from the 77 subjects were analysed for expression of 12 miRNAs (let-7a, let-7f, miR-19a, miR-22, miR26a, miR28-5p, miR-99b, miR151-5p, miR-221, miR-532-3p, miR-548-3p, miR-766). [score:3]
72(−1.12, -0.49)−0.79(−0.97, -0.48)−0.04(−0.19, 0.25)miR-2210.03(−0.32, 0.29)0.09(−0.21, 0.27)0.13(−0.21, 0.29)0.02(−0.27, 0.26)−0.28(−0.58, 0.10)−0.32(−0.53, 0.10)miR-26a2.07(1.90, 2.24)2.09(1.81, 2. 25)−0.02(−0.29, 0.26)1.94(1.70, 2.11)1.83(1.53, 2.15)−0.05(−0.39, 0.25)miR-28-5p−4.10(−4.51, -3.66)−4.11(−4.48, -3.71)0.09(−0.60, 0.53)−4.14(−4.63, -3.93)−4.30(−4.55, -3.95)−0.14(−0.76, 0.32)miR-532-3p−4.80(−5. [score:1]
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[+] score: 4
After successful adaptation of the previously developed transient miRNA mimics transfection protocol employing ScreenFect [®]A [25], cell type specific screening controls were established by transfecting functional control siRNAs including a non -targeting siRNA (NT), a human cell death inducing siRNA (DT) as well as the two already known pro-apoptotic miRNAs miR-137-3p (T98G, S KOV3, SGBS) and miR-28-5p (HCT 116 ) as positive controls. [score:3]
The functionality of the screening procedure was assured by using the pro-apoptotic miRNAs miR-137-3p and miR-28-5p as functional controls [43, 44]. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-1-2, hsa-mir-206, hsa-mir-1-1, hsa-mir-200a
For example, in breast cancer, miR-28 regulates NRF2 expression through a KEAP1-independent mechanism (29). [score:4]
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[+] score: 4
miRNA profiling of 80 type 2 diabetic patients compared with age and gender matched controls showed overexpression of miR-28-3p and underexpression of 12 miRNAs (miR-223, miR-320, miR-486, miR-150, miR-24, miR-21, miR-29b, miR-20b, miR-15a, miR-126, miR-191, and miR-197). [score:4]
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[+] score: 4
Overall, the 40 combinations consisted of 15 different miRNAs (miR-20b, miR-24, miR-28-3p, miR-132-3p, miR-140-3p, miR-146b-5p, miR-155, miR-191, miR-193a-5p, miR-328, miR-331, miR-381, miR-532, miR-628-5p, and miR-660) that were used for further analysis. [score:1]
The three identified candidate references miR-20b, miR-28-3p, and miR-146b-5p showed no statistically significant differences between asbestos-exposed controls and mesothelioma patients. [score:1]
No significant fold changes > 2.0 could be observed for miR-24, miR-28-3p, miR-132-3p, and miR-146b-5p at low hemolysis grades < 0.5% (Figure 2 and Additional File 3). [score:1]
Thus, miR-20b, miR-28-3p, and miR-146b-5p and the four combinations (GM of miR-20b/miR-28-3p, miR-20b/miR-146b-5p, miR-28-3p/miR-146b-5p, and miR-20b/miR-28-3p/miR-146b-5p) were in principal feasible as potential references for subsequent analyses. [score:1]
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[+] score: 4
There were however seven microRNAs (miR-335-3p, miR-128, miR-224-5p, miR-28-5p, miR-191-5p, miR-423-3p, and miR-181a-5p) with a statistically significant upregulation in the controls. [score:4]
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[+] score: 4
Of these, only miR-28 and miR-144a have been experimentally proven to directly target and repress NRF2 mRNA [29, 30]. [score:4]
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55
[+] score: 4
Other miRNAs from this paper: hsa-mir-25, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
In the miR-28 network (Figure 8C), ASF/SF2 expression is modulated by miR-28 and miR-505 (not show here) which are negatively controlled by LRF to influence the proliferation and survival of mouse embryonic fibroblasts [75]. [score:3]
The functional networks of miR-92b (PRdmiR, mir-25 family, derived from GC rich tandem repeats), miR-28 (RdmiR, mir-28 family, derived from LINE), miR-151 (RdmiR, mir-28 family, derived from LINE), miR-421 (RdmiR, mir-95 family, derived from LINE), miR-1271 (RdmiR, mir-1271 family, derived from LINE), miR-340 (RdmiR, mir-340 family, derived from DNA transportable element) and miR-378 (RdmiR, mir-378 family, derived from SINE) have been reconstructed (Figure 8). [score:1]
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56
[+] score: 3
Human immunodeficiency virus-1 mRNA is suppressed by a cluster of miRNAs, including miR-28, miR-125b, miR-150, miR-223 and miR-382 (9). [score:3]
[1 to 20 of 1 sentences]
57
[+] score: 3
Whereas, miR-28 expression was lower in type III latency. [score:3]
[1 to 20 of 1 sentences]
58
[+] score: 3
Other miRNAs from this paper: hsa-mir-708
Among them, has-miR-708-5p and has-miR-28-5p have high expression in human brain tissues [21]. [score:3]
[1 to 20 of 1 sentences]
59
[+] score: 3
MicroRNAs microRNA-15b, microRNA-16, microRNA-22, and microRNA-185 were found to have strong positive correlation with the appearance of erythroid surface antigens (CD71, CD36, and CD235a) and hemoglobin synthesis, while microRNA-28 displayed an inverse relationship with the expression of these markers. [score:3]
[1 to 20 of 1 sentences]
60
[+] score: 3
For the Per genes we find that Per1 is a weakly predicted target for 2 of the fluctuating plasma miRNAs, miR-28-3p and miR-103a-3p, discovered in the present study while Per2 is predicted to interact weakly with miR-24-3p and miR-363-3p. [score:3]
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61
[+] score: 3
Deng et al. 36 performed a study in healthy male coke oven workers to identify miRNAs associated with PAH exposure, and found that urinary 4-hydroxyphenanthrene and/or plasma BPDE–Alb adducts were associated with lower miR-24-3p, miR-27a-3p, miR-142-5p, and miR-28-5p expression. [score:3]
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62
[+] score: 3
The ceRNA pair MEG3-MCL1 putatively shares 16 common miRNAs including miR-28, miR-181d, miR-520a, miR-520b and miR-876-3p and show comparable high co -expressions in breast and colon, especially in colon (MEG3 (66.2): MCL1 (37.9)). [score:3]
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63
[+] score: 3
Bai X. T. Nicot C. miR-28-3p is a cellular restriction factor that inhibits human T cell leukemia virus, type 1 (HTLV-1) replication and virus infection J. Biol. [score:3]
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64
[+] score: 3
Other miRNAs from this paper: hsa-mir-433, hsa-mir-493
Besides our current results on miR-493-3p, also miR-433-3p [17] and miR-28-5p [45, 46] have recently been reported to target Mad2 mRNA. [score:3]
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65
[+] score: 3
MicroRNAs miR-15b, miR-16, miR-22, and miR-185 were found to have strong positive correlation with the appearance of erythroid surface antigens (CD71, CD36, and CD235a) and hemoglobin synthesis, while miR-28 displayed an inverse relationship with the expression of these markers [7]. [score:3]
[1 to 20 of 1 sentences]
66
[+] score: 3
In the 2q21 band genes are located which relate to the cellular cycle control (CCNT2, MAP3K19 and MZT2A), DNA replication/repair mechanisms (ERCC3, MCM6), proto-oncogene (MIR28 and RAB6C) and tumor suppressor genes (CXCR4 and NMTC1). [score:3]
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67
[+] score: 3
Other miRNAs from this paper: hsa-mir-409, hsa-mir-625
Among these differentially expressed miRNAs, several have been reported in previous studies, such as miRlet-7, miR409, miR-28-5p, miR-625, etc. [score:3]
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68
[+] score: 3
[19] Likewise, only two miRNAs (hsa-miR-220c-3p and hsa-miR-28-5p) showed altered expression in T-lymphocyte cell lines following 15 days of incubation with chlorpromazine, haloperidol and clozapine. [score:3]
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69
[+] score: 3
Huang et al. reported that a cluster of cellular miRNAs, including miR-28, miR-125b, miR-150, miR-223 and miR-382, targets the 3′ ends of various human immunodeficiency virus 1 (HIV-1) mRNAs. [score:3]
[1 to 20 of 1 sentences]
70
[+] score: 3
In turn, the cytoplasmic miRNA cluster, consisting of miR-28, miR-125b, miR-150, miR-223 and miR-382 molecules, interacts with human immunodeficiency 1 virus (HIV-1) in non-activated T CD4+ lymphocytes and inhibits its multiplication [87]. [score:3]
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71
[+] score: 3
In addition, Nrf-2 has been recently demonstrated to be regulated by miR-28 in non-neuronal mo dels, and miR-144, 153, 27a and 142–5p in neurons [17– 19]. [score:2]
Endogenous level of miR-28, 142–5p and 144 showed no obvious change between GSCs and non-GSCs glioma cells. [score:1]
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72
[+] score: 2
Finally, among the 64 miRNAs, four (miR-28, miR-331, miR-486 and miR-502) were differently deregulated at, at least, two different time points of infection. [score:2]
[1 to 20 of 1 sentences]
73
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Spinal cord miR-28, miR-217, miR-218-1, miR-329, miR-331. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
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74
[+] score: 2
Notably, five significantly deregulated miRNAs, i. e., miR-9 (1q23.2), miR-15b (3q25.32), miR-28-5p (3q27.3), miR-100 and miR-125b (11q24.1) have been found to be associated with recurrent chromosomal alterations [92]. [score:2]
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75
[+] score: 2
Finally, although a moderate significance of the ANOVA test between WT and mutant cell lines (p<0.07) due to the high background of NIH3T3 cell lines, 11 miRNA were specifically related to the presence of a hemizygous or heterozygous KIT mutation: miR-19b, miR-26a, miR-26b, miR-28-3p, miR-29a, miR-29b, miR-100, miR-192, miR-218, miR-222, and miR-708. [score:2]
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76
[+] score: 1
To add to this intriguing interplay between cellular miRNAs and viral pathogens, Huang and colleagues has demonstrated that HIV, an enveloped RNA virus of the Retreoviridae family utilise host cellular miR-28, miR-125b, miR-150, miR-223 and miR-382 to control viral protein synthesis in order to evade host immune system [47]. [score:1]
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77
[+] score: 1
In the Figure, the red arrows (for miR-19a-3p, miR-28-5p and miR-301-3p) indicate these sequences are mapped to the genome sequence with one mismatch. [score:1]
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78
[+] score: 1
Other miRNAs from this paper: hsa-mir-17, hsa-mir-223, hsa-mir-127, hsa-mir-188, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-30e, hsa-mir-362, hsa-mir-363, hsa-mir-367, hsa-mir-379, hsa-mir-196b, hsa-mir-450a-1, hsa-mir-431, ssc-mir-28, hsa-mir-493, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-500a, hsa-mir-501, hsa-mir-502, hsa-mir-450a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-506, hsa-mir-508, hsa-mir-509-1, hsa-mir-532, hsa-mir-615, hsa-mir-660, bta-mir-127, bta-mir-30e, bta-mir-17, bta-mir-450a-2, bta-mir-532, bta-mir-363, bta-mir-660, hsa-mir-891a, hsa-mir-892a, hsa-mir-509-2, hsa-mir-450b, hsa-mir-892b, hsa-mir-708, hsa-mir-509-3, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1248, ssc-mir-17, bta-mir-155, bta-mir-188, bta-mir-194-2, bta-mir-196b, bta-mir-223, bta-mir-28, bta-mir-362, bta-mir-367, bta-mir-379, bta-mir-431, bta-mir-493, bta-mir-500, bta-mir-502a-1, bta-mir-502a-2, bta-mir-502b, bta-mir-615, bta-mir-708, bta-mir-1248-1, bta-mir-1248-2, ssc-mir-450a, bta-mir-2320, bta-mir-1388, bta-mir-194-1, bta-mir-450a-1, eca-mir-30e, eca-mir-367, eca-mir-684, eca-mir-196b, eca-mir-615, eca-mir-708, eca-mir-194-1, eca-mir-493a, eca-mir-17, eca-mir-1248, eca-mir-28, eca-mir-127, eca-mir-379, eca-mir-431, eca-mir-493b, eca-mir-155, eca-mir-194-2, eca-mir-188, eca-mir-223, eca-mir-362, eca-mir-363, eca-mir-450a, eca-mir-450b, eca-mir-450c, eca-mir-500-1, eca-mir-500-2, eca-mir-501, eca-mir-502, eca-mir-508, eca-mir-509a, eca-mir-532, eca-mir-660, ssc-mir-30e, ssc-mir-196b-1, ssc-mir-450b, ssc-mir-127, ssc-mir-532, ssc-mir-708, ssc-mir-1285, ssc-mir-500, hsa-mir-514b, ssc-mir-363-1, ssc-mir-450c, hsa-mir-500b, ssc-mir-194b, ssc-mir-155, ssc-mir-362, bta-mir-3601, ssc-mir-615, ssc-mir-2320, bta-mir-450b, ssc-mir-194a, ssc-mir-196b-2, ssc-mir-363-2, ssc-mir-493, hsa-mir-892c, eca-mir-1388, eca-mir-514b, eca-mir-506a, eca-mir-509b, bta-mir-194b, ssc-mir-1388, ssc-mir-223, ssc-mir-660, bta-mir-194b-2, bta-mir-1949
The reason is that at least some Rfam miRNA families are inconsistent with miRBase (an example is mir-28, mir-708 where high confident BLAST Rfam hits are observed on the same locations on opposite strands, however miRBase only match one of the two families to a given location and the families are only weakly related. [score:1]
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79
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Of these, while 24 miRNAs including miR150, miR199a-5p, miR-223, miR-28-5p, miR-451, were significantly depleted, 10 miRNAs including miR-34a, miR-155, miR-193b, miR-365, miR-551b, displayed induction. [score:1]
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80
[+] score: 1
66 hsa-miR-511 −4.05 16.61 hsa-miR-26b −4.01 16.15 hsa-miR-210 −4.01 16.15 hsa-miR-489 −3.98 15.78 hsa-miR-22* −3.98 15.74 hsa-miR-15a* −3.97 15.70 hsa-miR-106a −3.92 15.15 hsa-miR-331-5p −3.91 15.04 hsa-miR-194 −3.88 14.73 hsa-miR-139-5p −3.85 14.38 hsa-miR-193a-5p −3.84 14.37 hsa-miR-29a −3.80 13.94 hsa-miR-24 −3.75 13.43 hsa-miR-140-5p −3.71 13.12 hsa-miR-28-3p −3.69 12.91 hsa-miR-151-3p −3.67 12. [score:1]
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81
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Bioinformatic approaches were used to validate six of the eight top-candidate microRNAs, which were miR-28, miR-34a, and four members of the miR-30 family (miR-30c-1, miR-30b, miR-30d, and miR-30c-2) [10]. [score:1]
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82
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In another study, in premenopausal women and their monozygotic postmenopausal twins using estrogenic HRT, other circulating miRNAs included in exosomes, such as miR-148a-3p, miR-27-3p, miR-28-3p, miR-30a-5p, miR-106b-5p, and miR-126-5p were associated with serum estradiol levels [94]. [score:1]
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83
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Strand-specific miR-28-5p and miR-28-3p have distinct effects in colorectal cancer cells. [score:1]
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84
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The analysis with the tool edgeR showed following differenced in contrast to the analysis with DESeq2: four miRNAs were not significantly affected by the level of hemolysis (eca-miR-744, eca-miR-128, eca-miR-28-3p and eca-miR-125a-5p) and additionally five significantly affected miRNAs were reported: eca-miR-423-5p, eca-let-7g, eca-miR-19b, eca-miR-425, eca-miR-7177b (Table S6). [score:1]
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85
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mir-616 and mir-28 are derived from transposed elements (LINE, L2 family) [29] and are located within two translocation breakpoints, respectively DDIT3, that is often fused to FUS in myxoid liposarcoma [30], and LPP, that is fused to MLL in a secondary acute leukemia [31]. [score:1]
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86
[+] score: 1
The miR-28-5p and miR-28-3p also play opposite roles in colon cancer cell proliferation and migration (36). [score:1]
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87
[+] score: 1
For instance, mir-28, mir-95 and mir-151 are derived from LINE-2 TEs, and mir-548 family is derived from Made1 TEs [21– 23]. [score:1]
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88
[+] score: 1
Other miRNAs from this paper: hsa-mir-505
A recent study shows that LRF represses the microRNAs miR-28 and miR-505 [22]. [score:1]
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89
[+] score: 1
Of these, binding sites for miR-23, miR-218 and miR-338 were found conserved in the 3′UTR of elephant shark Runx2, while only that for miR-28 is present in zebrafish and fugu Runx2 (Fig. 8B). [score:1]
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90
[+] score: 1
For instance, the miRNA-28 family originates from LINE L2B elements. [score:1]
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