sort by

37 publications mentioning mmu-mir-296

Open access articles that are associated with the species Mus musculus and mention the gene name mir-296. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 172
We identified 1 validated target of miR-296-3p; 5 validated targets of miR-298-5p; 207 predicted targets of miR-296-3p; 707 predicted targets of miR-298-5p. [score:9]
Four of them (HMX2, HNF4A, LEF1, MAFB) are known to be expressed in the islets of Langerhans, and MAFB is known to be expressed only in rodent islet α cells within adult pancreas [25]; the presence of binding sites for this TF within the promoter of the genes encoding miR-296-3p and miR-298-5p suggests that it may regulate the expression of both miRNAs. [score:8]
Altogether, high-throughput microRNA profiling, functional analysis with synthetic mimics and molecular characterization of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p, coupled to upregulation of their targets as IGF1Rβ and TNFα, is a major determinant of mammalian pancreatic α cells resistance to apoptosis induction by cytokines. [score:7]
HT miRNA profiling data, functional analysis with synthetic mimics and molecular characterisation of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p in pancreatic α cells, coupled to upregulation of their targets as IGF1Rβ and TNFα and activation of the corresponding signaling pathways, is a major determinant of their resistance to apoptosis induction by cytokines. [score:7]
Within the network of genes regulated by α-miRNAs, insulin-like growth factor receptor signaling pathway is a biological process significantly enriched among the genes interacting with targets of miR-296-3p and miR-298-5p, with respect to the genes linked to the targets of the other miRNAs (p-value = 0.039, Fisher’s exact test). [score:6]
Among them, Bcl2, Ccna2, Irs2, Nr4a2 are transcriptionally regulated by CREB1, which is a validated target of miR-296-3p [22]; Tnf and Vdr are validated targets of miR-298-5p [23, 24]. [score:6]
We focused our study on two microRNAs, miR-296-3p and miR-298-5p, which were: (1) specifically expressed at steady state in αTC1-6, but not in βTC1 or INS-1 cells; (2) significantly downregulated in αTC1-6 cells after treatment with cytokines in comparison to untreated controls. [score:6]
Modulation of miR-296-3p and miR-298-5p also alters expression of their targets. [score:5]
To verify whether in vitro modulation of miR-296-3p and miR-298-5p affected the expression of their targets, we performed transient transfection experiments of αTC1-6 cells with their mimics. [score:5]
Our computational analysis suggests that MAFB (a transcription factor exclusively expressed in pancreatic α cells within adult rodent islets of Langerhans) controls the expression of miR-296-3p and miR-298-5p. [score:5]
Figure 4 Modulation of miR-296-3p and miR-298-5p alters expression of their targets. [score:5]
Although its biological effect was potentiated when also miR-296-3p was expressed, our results suggest that the role of miR-298-5p is more important in this process than that of miR-296-3p (Figure  3): this would highlight the role of one or a few specific miR-298-5p targets. [score:5]
Bar graph showing changes in gene expression of a selected set of miR-296-3p and miR-298-5p targets for each of three different experimental conditions: (i) αTC1-6 treated with cytokines with respect to matched untreated control cells at the time points 24 and 48 h; (ii) untreated αTC1-6 transfected with mimics of miR-296-3p with respect to scramble -transfected control cells at the time points 24 and 48 h; (iii) untreated αTC1-6 transfected with mimics of miR-298-5p with respect to scramble -transfected control cells at the time points 24 and 48 h. Data are reported as LOG of 2^ [-ΔΔCt] values. [score:5]
Single TaqMan gene expression assays (STAs) during a time course analysis (6-12-24-48 h) showed a highly significant downregulation of miR-296-3p in αTC1-6 cells at 24 and 48 h PT, compared to matched untreated controls (Student’s t-test, Bonferroni adjusted p-value < 0.01). [score:4]
By exploiting specific microRNA mimics, we demonstrated that experimental upregulation of miR-296-3p and miR-298-5p raised the propensity to apoptosis of transfected and cytokine -treated αTC1-6 cells with respect to αTC1-6 cells, treated with cytokines after transfection with scramble molecules. [score:4]
Figure 3 Upregulation of miR-296-3p and miR-298-5p reduces αTC1-6 resistance to apoptosis induced by cytokines. [score:4]
Figure 5 Expression of IGF1Rβ and TNFα proteins is regulated by miR-296-3p and miR-298-5p in αTC1-6. (A) of IGF1Rβ in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (middle); (3) αTC1-6 treated with cytokines for 24 h and their matched untreated controls (right). [score:4]
Expression of IGF1Rβ and TNFα is controlled by miR-296-3p and miR-298-5p in αTC1-6 cells. [score:3]
Decreased expression of mir-296-3p and miR-298-5p and the corresponding activation of survival and proliferation signals, mediated by IGF1R and its downstream nodes (e. g., IRS-1 and ERK-1), may thus explain why αTC1-6 cells are resistant to death induction by cytokines (see Additional file 13). [score:3]
Through western analysis, we confirmed our computational prediction that IGF1Rβ and TNFα are common targets to both miRNAs and that miR-296-3p and miR-298-5p also control IRS-1 and ERK-1 within the IGF1R signaling pathway. [score:3]
The expression of phospho-IRS-1 didn’t change in untreated αTC1-6 transfected with mimics of each miRNA alone, while it decreased about 1.5 folds in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p (Figure  6A, left panel). [score:3]
Figure 2 Expression of miR-296-3p and miR-298-5p in αTC1-6 and βTC1. [score:3]
Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
We focused our attention on 7 targets of miR-296-3p, 4 of miR-298-5p, 2 common to both miRNAs: they were chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion (see Additional file 8). [score:3]
Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
Identification of miR-296-3p and miR-298-5p targets. [score:3]
In αTC1 transfected with mimics of miR-296-3p or miR-298-5p, real-time PCR showed altered expression of different genes with respect to scramble -transfected cells, including Igf1r, Tnf, Vdr (Figure  4). [score:3]
Click here for file Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
A selection of validated and predicted targets of miR-296-3p and miR-298-5p was chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion. [score:3]
Click here for file Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
Following transfection of αTC1-6 with either mimics of miR-296-3p or miR-298-5p, TNFα protein was about 1.2 folds less expressed with respect to scramble -transfected controls; this decrease was more pronounced (1.6 folds) when cells were transfected with both mimics (Figure  5B, left panel). [score:3]
Expression of a macro-noncoding RNA (precursor of miR-296, miR-298, Nespas) is predicted to be controlled by two groups of CpG islands (one comprising two CpG islands, from 17.5 to 18.8 kb upstream the first nucleotide of pre-miR-296; the other made of three CpG islands, from 30.1 to 33.6 Kb upstream the first nucleotide of pre-miR-296). [score:3]
Interestingly, also the activation of ERK-1 appears to be regulated by miR-296-3p and miR-298-5p: in the absence of treatment with cytokines, αTC1-6 cells transfected with mimics of miR-296-3p showed levels of phospho-ERK-1 (Thr202) similar to those found in scramble -transfected αTC1-6 cells; the transfection with mimics of miR-298-5p or of both miRNAs led instead to a decrease of the protein (1.2 and 1.3 folds, respectively) (Figure  6B, left panel). [score:2]
Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Phospho-IRS1 (Tyr612) and Phospho-ERK-1 (Thr202), which we demonstrated to be controlled by miR-296-3p and miR-298-5p, are known to regulate the response to insulin and to be involved in survival and proliferation processes [30]. [score:2]
Click here for file 3 Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Transient transfection of αTC1-6 cells with mimics of miR-296-3p and miR-298-5p. [score:1]
αTC1-6 transfection with mimics of miR-296-3p and miR-298-5p increases apoptosis levels induced by cytokines. [score:1]
By using the same controls, we detected a slight decrease of phospho-IRS-1 (1.2 folds) in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p and treated with cytokines (Figure  6A, right panel). [score:1]
On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
At 24 h PT, αTC1-6 transfected with mimics of miR-298-5p show a highly significant increase of the number of apoptotic cells with respect to scramble -transfected control; at the same time point, in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p a highly significant increase of the number of apoptotic cells is detected with respect to all the other experimental conditions. [score:1]
Transfections were performed using siPORT™ NeoFX™ (Lifetechnologies™) with 30 nM mimics of miR-296-3p/miR-298-5p/scrambled sequence (Pre-miR™ miRNA Precursor Molecules—Negative Control #1, Lifetechnologies™). [score:1]
Figure 6 Activation of IRS-1 and ERK-1 is under control of miR-296-3p and miR-298-5p in αTC1-6. (A) of phospho-IRS-1 (Tyr612) in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (right). [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islands. [score:1]
Among them, miR-296-3p and miR-298-5p stood out clearly as potentially critical nodes, responsible for α cells resistance to cytokine -induced cell death. [score:1]
Sequences of mature miR-296-3p are 100% conserved between rodents and humans, whereas those of miR-298-5p are 74% identical. [score:1]
CpG islands upstream genes encoding miR-296, miR-298, Nespas were identified through UCSC Genome Browser (http://genome. [score:1]
Our results suggest that miR-296-3p and miR-298-5p play a pivotal role in determining this trait. [score:1]
The decrease of IGF1Rβ was not detectable in αTC1-6 transfected with either mimic of miR-296-3p or miR-298-5p and then treated with cytokines for 24 h. In αTC1-6 treated with cytokines for 24 h, after transfection with mimics of both miRNAs 296-3p and 298-5p, it was instead lower than at steady state (1.4 folds). [score:1]
In the genomic region comprising the genes encoding miR-296-3p, miR-298-5p and Nespas, MatInspector identified Transcription Factor Binding Sites (TFBS) for sixty seven Transcription Factors (TFs). [score:1]
Activation of IRS-1 and ERK-1 is also under control of miR-296-3p and miR-298-5p. [score:1]
Finally, χ [2]-square test was used to establish if miR-296-3p and miR-298-5p have more common targets than expected by chance; Fisher’s exact test was applied to evaluate the enrichment in specific gene ontologies. [score:1]
Analysis of this region through UCSC browser revealed the presence of two clusters of CpG islands: (i) one comprises two CpG islands, from 17.5 to 18.8 kb upstream the first nucleotide of pre-miR-296, and is located 9.2 and 10 Kb downstream Nespas transcription start site (TSS); (ii) the other is made of three CpG islands from 30.1 to 33.6 Kb upstream the first nucleotide of pre-miR-296 and is located 1.8-5 kb upstream Nespas TSS (see Additional file 7). [score:1]
For each time point DCt values of miR-296-3p and miR-298-5p were correlated, both from untreated and cytokines -treated αTC1-6 cells (r-value = 0.88, p-value = 1.15e-08, Pearson’s correlation test). [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islandsGenes encoding miRNAs 296-3p and 298-5p are clustered in a genomic region, which also comprises the gene for the noncoding transcript Nespas and is imprinted in mice and humans [21]. [score:1]
For analysis of correlation between the expression of miR-296-3p and miR-298-5p in αTC1-6, Pearson correlation coefficient was calculated. [score:1]
The percentage of apoptotic αTC1-6 cells after transfection with mimics of miR-296-3p was comparable to scramble -transfected controls during the entire time course treatment. [score:1]
Click here for file On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
org predicts two binding sites for mmu-miR-296-3p and mmu-miR-298-5p on Mafb mRNA 3’ UTR. [score:1]
Their assignment to specific families is shown in Additional file 5. To identify miRNAs whose functions could explain the differential response to cytokines of pancreatic α and β cells, we specifically focused our attention on miR-296-3p and miR-298-5p. [score:1]
[1 to 20 of 60 sentences]
2
[+] score: 55
Sperm showed significantly higher (P<0.001) expression of imprinted and paternally expressed miRNAs (miR-296-3p, miR-296-5p, miR-483) and lower (P<0.001) expression of imprinted and maternally expressed miRNAs (miR-127, miR-127-5p) than those observed with somatic cells (Figure 1B). [score:9]
Using mouse as a mo del system, here we show that, similar to sperm, expression of imprinted and paternally expressed miRNAs (miR-296-3p, miR-296-5p, miR-483) were consistently higher (P<0.001), while those of imprinted and maternally expressed miRNA (miR-127, miR-127-5p) were consistently lower (P<0.001) in GS cells than in control embryonic stem (ES) cells. [score:7]
Similar to sperm, the expression of imprinted and paternally expressed miRNAs (miR-296-3p, miR-296-5p, miR-483) were consistently higher (P<0.001) while those of imprinted and maternally expressed miRNA (miR-127, miR-127-5p) were consistently lower (P<0.001) in GS cells than in control ES cells (Figure 2). [score:7]
The miR-296 regulates the expression of growth factor receptor in endothelial cells [56] and increases upon in vitro differentiation of ES cells to target the Nanog gene transcript [57]. [score:6]
However, their expression pattern differed among the differentiating cells of the three groups (Figure 4A and 4B) and, the EBs generated from GS cells resembled those of ES cells for the expression pattern of miR-296-3p. [score:5]
On the other hand, Gnas-Nespas DMR is imprinted (i. e., DNA methylated) on maternal chromosome to suppress the expression of miR-296 from maternal chromosome [14], [15], [30]. [score:5]
Expression of miR-296-3p (A), miR-296-5p (B), miR-127 (C), miR-127-5p (D) and miR-483 (E) imprinted miRNAs during in vitro differentiation of male germ-line (GS) and multipotent adult germ-line (maGS) stem cells. [score:3]
Expressions of miR-296-3p, miR-296-5p, miR-127, miR-127-5p and miR-483 imprinted miRNAs in male germ-line (GS) and multipotent adult germ-line (maGS) stem cells. [score:3]
B: Expression of miR-296-3p, miR-296-5p, miR-127, miR-127-5p and miR-483 imprinted miRNAs in mouse somatic cells (open box), sperm (crossed box) and testis-tissue (closed box). [score:3]
both) occurs in a tissue -dependent manner [45], [46], [47], the differences in the expression of miR-296-3p and miR-296-5p among the EBs of the three groups probably reflects the different proportion of cells of three germ-layers in them [11], [39], [40], [41]. [score:3]
Three imprinted miRNAs, miR-127, miR-483 and miR-296, which are encoded from Dlk1-Dio3, Igf2-H19 and Gnas-Nespas imprinted gene clusters, respectively under the regulation of common ICRs (Dlk1-Dio3 IG-DMR, Igf2-H19 ICR and Gnas-Nespas DMR) for all miRNAs in the respective gene clusters were analyzed (Figure 1A) [20], [30], [31], [32]. [score:2]
We also observed that, similar to previous reports on several miRNAs [45], [46], mature miRNA originating from both 3′ (miR-296-3p) and 5′ (miR-296-5p) arms of the miR-296 accumulated as sister pairs in undifferentiated testis-derived germ-line stem cells (Figure 1B). [score:1]
On the other hand, Gnas-Nespas cluster encode miR-296 and miR-298 which are derived from non-coding Nespas gene transcript. [score:1]
[1 to 20 of 13 sentences]
3
[+] score: 36
Regarding these observations, we performed qRT-PCR for 8 target genes of commonly regulated miRNA; 4 target genes (ATG5, ITGA6, NCKAP1, SARBS1) of the 2 up-regulated miRNA (mmu-miR-291b-5p, mmu-miR-296-5p) and 4 target genes (AKT1, APC, LMO7, MSN) of the 3 down-regulated miRNA (mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*). [score:14]
Interestingly, in cluster A, 3 miRNAs (mmu-miR-30c-1*, mmu-miR-374* and mmu-miR-497b*) were identified as being down-regulated by all nine polyphenols tested, while in cluster 2, 2 miRNAs (mmu-miR-291b-5p and mmu-miR-296-5p) were observed as up-regulated by all nine polyphenols (Table 2). [score:7]
Regarding miR-296-5p, its expression has been observed to be down-regulated in endothelial cells exposed to inflammatory stimulus [30]. [score:6]
Different studies have been reported regarding miR-296 for which the expression has been observed to be down-regulated in the mouse brain after prenatal ethanol exposure and has been shown to be associated with mental retardation [31], or parathyroid cancer tissue [32] or even NIH3T3 cells exposed to UV irradiation that induces apoptosis and necrosis. [score:6]
Moreover, changes in miRNA expression were observed after polyphenol supplementation, and five miRNAs (mmu-miR-291b-5p, mmu-miR-296-5p, mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*) were identified as being commonly modulated by these polyphenols. [score:3]
[1 to 20 of 5 sentences]
4
[+] score: 19
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
DEX treatment up-regulated the expression of miRNA-483, miRNA-181a-1, miRNA-490 and miRNA-181b-1, while it down-regulated the levels of miR-122, miR-466b, miR-200b, miR-877, miR-296, miRNA-27a and precursor of miR-504. [score:9]
In contrast, dexamethasone down-regulated the expression of several of the miRNAs by more than 1.5 fold, i. e., miR-122 (8.2-fold), miR-466b (2.31-fold), miR-200b (1.9-fold) miR-877 (1.61-fold), miR-296 (1.61-fold)and precursor of miR-504 (1.53-fold) (Fig. 2D ). [score:6]
miR-296 and miR-122 were down-regulated (>1.5 fold) by both 17α-E2 and DEX. [score:4]
[1 to 20 of 3 sentences]
5
[+] score: 17
The expression pattern observed for mmu-miR-296-5p (down regulated by 25-fold between 2 days and 12 weeks of age) supports a potential role as an utrophin suppressor during myofibre maturation. [score:6]
Mmu-miR-296-5p overexpression almost totally suppresses the utrophin-A protein in C2C12 myoblasts [69]. [score:5]
b Box-plots of miRNA expression levels of mmu-miR-134-5p, mmu-miR-136-5p, mmu-miR-214-3p, mmu-miR-296-5p in mouse quadriceps muscle at 2 days, 2 weeks, 4 weeks and 12 weeks after birth. [score:3]
Of interest, all 4 top-ranked miRNAs in cluster B were predicted to target one of the Pax gene family members with a high degree of certainty, potentially indicating a similar role for mmu-miR-134-5p, mmu-miR-136-5p and mmu-miR-296-5p. [score:3]
[1 to 20 of 4 sentences]
6
[+] score: 16
Of these, 12 (mir-9, mir-200c, mir-708, mir-377, mir-26b, mir-296, mir-369, mir-32, mir-1965, mir-1190, mir-135b and mir-201) were differentially up-regulated and five (mir-291a, mir-190b, mir-297c, mir-713 and mir-470) were differentially down-regulated. [score:7]
The up-regulated miRNAs, including miR-708, miR-296, miR-200c, miR-377 and miR-1190, were all strongly predicted to affect target genes involved in the MAPK pathway. [score:6]
Mitogen-activated protein kinase (MAPK) signaling pathway was one of the most significant pathways to be affected by 74 target genes of miR-708, miR-296, miR-200c, miR-377 and miR-1190 (Table 1). [score:3]
[1 to 20 of 3 sentences]
7
[+] score: 15
To correct (to the extent possible) for this difference, we excluded a further 20 target sites with GU pairs and mismatches in the seed region for miR-134, and 8 target sites for miR-296 (all target sites for miR-375 have WC matches in the seed region), and report the results of 65 target genes examined for miR-134, 6 for miR-296 (for miR-296, all six sites examined were validated), and 22 for miR-375. [score:9]
miRNA Condition Number of targets miR-134 WC bp at nt 2–7 True positives 43 Sensitivity = 0.551 False negatives 35 Specificity = 0.666 False positives 3 True negatives 6 Total 87 WC bp at nt 2–7, and 40% FE threshold (−18.64) True positives 36 Sensitivity = 0.462 False negatives 42 Specificity = 0.666 False positives 3 True negatives 6 Total 87 miR-296 WC bp at nt 2–7 True positives 8 Sensitivity = 0.80 False negatives 2 Specificity = 0.50 False positives 1 True negatives 1 Total 12 WC bp at nt 2–7, and 40% FE threshold (−19.44) True positives 7 Sensitivity = 0.70 False negatives 3 Specificity = 0.50 False positives 1 True negatives 1 Total 12 miR-375 WC bp at nt 2–7 True positives 9 Sensitivity = 0.375 False negatives 15 Specificity = 0.929 False positives 1 True negatives 13 Total 38 WC bp at nt 2–7, and 40% FE threshold (−16.68) True positives 8 Sensitivity = 0.333 False negatives 16 Specificity = 0.929 False positives 1 True negatives 13 Total 38Of 158 genes experimentally tested for regulation by miR-134, 85 occur in our database, as do 14 of 24 tested for regulation by miR-296, and 22 of 44 tested for regulation by miR-375. [score:6]
[1 to 20 of 2 sentences]
8
[+] score: 13
Other miRNAs from this paper: mmu-mir-302a, mmu-mir-17, mmu-mir-302d
For instance, RT-qPCR showed that miR-296 was significantly downregulated (Figure 4(f)). [score:4]
To examine miR-296 function in PD -induced Nanog expression, we subcloned coding sequence (CDS) fragment of Nanog downstream the reporter gene in the psiCHECK-2 vector (Figure 5(e), upper panel). [score:3]
Furthermore, western blot and RT-qPCR showed that transfection of miR-296 mimics suppressed Nanog levels in J1 mESCs (Figures 5(f) and 5(g)); however PD can compromise miR-296 reduction on Nanog (Figure 5(f)). [score:3]
Luciferase assays were performed by cotransfection of the reporter vector and miR-296 mimics into 293T cells for 24 h. As shown in Figure 5(e), the reporter that harbored the CDS fragment of Nanog was significantly repressed, whereas miR-296 inhibitor could rescue luciferase activity. [score:2]
The miR-296-5p mimics were purchased from Shanghai GenePharma (Shanghai, China). [score:1]
[1 to 20 of 5 sentences]
9
[+] score: 12
However, Barbagallo et al. reported that the downregulation of miR-296-3p and miR-298-5p, which consequently led to the upregulation of their respective targets IGF1Rβ and TNFα, was a major determinant of the resistance of mammalian pancreatic α cells to cytokine -induced apoptosis [27]. [score:9]
Nevertheless, we did not observe the differential expression of miR-296-3p after scrotal hyperthermia. [score:3]
[1 to 20 of 2 sentences]
10
[+] score: 10
CD3 [+] peripheral T lymphocytes exhibited two modulated miRNAs, miR-296-5p (down-regulated) and miR-378 (up-regulated), and PILs exhibited seven upregulated miRNAs (miR 202-3p, miR 709, miR 10b*, miR 705, miR 697, miR 712 and miR 877). [score:10]
[1 to 20 of 1 sentences]
11
[+] score: 10
However, circulating levels of miR-296 and miR-433 were found to be downregulated in hypertension and congenital heart disease, respectively [56, 57]. [score:6]
Few of the highly upregulated microRNAs were: miR-79, miR-183, miR-206, miR-207, miR-296-3p, miR-298, miR-380-5p, miR-433, miR-449b, miR-705, miR-761 (S1 Table). [score:4]
[1 to 20 of 2 sentences]
12
[+] score: 9
A recent study reported that PIN1 expression is regulated by the tumor suppressive miRNA miR-296-5p in prostate cancer [28]. [score:6]
However, aberrant mir-296-5p expression is rarely detected in NPC [29]. [score:3]
[1 to 20 of 2 sentences]
13
[+] score: 8
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 A) C2C12 myotubes were treated with 10ng/ml of TWEAK for 18h following isolation of total RNA enriched with small RNAs. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 In order to understand the interaction between different genes, we generated common networks using Ingenuity Pathway Analysis (IPA) software. [score:4]
[1 to 20 of 2 sentences]
14
[+] score: 8
RT-qPCR using TaqMan probes was performed in triplicate to determine the expression of miR-145, miR-296, miR-134, and miR-21, normalized to RNU6B expression, and reported as average differences in fold change from RNU6B expression. [score:7]
The levels of miR-134 and miR-296 were measured, because they are reported to target the coding sequence of Sox2 mRNA [37]. [score:1]
[1 to 20 of 2 sentences]
15
[+] score: 8
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-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-7a-3, 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-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, 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-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
expression increases in mouse ESCs treated with retinoic acid (RA), favoring ESCs differentiation into ectodermal lineages including neural cells by directly regulating the expression of the pluripotency factors Nanog and Sox2 and indirectly Oct4 in combination with miR-296 and miR-470 (Tay et al., 2008; Niu et al., 2013). [score:8]
[1 to 20 of 1 sentences]
16
[+] score: 7
Those down-regulated miRNAs included miR-134-5p, miR-296-3p, miR-381-3p, miR-449a-5p, miR-449c-5p, and miR-302 clusters. [score:4]
MiR-296 was up-regulated after RA treatment of mouse ES cell. [score:3]
[1 to 20 of 2 sentences]
17
[+] score: 6
For instance, among Dicer1 -dependent miRNAs, miR-210, miR-204, miR-672, miR-191 and miR-296 are predicted to regulate 13 distinct transcripts whose expression is significantly modified in the corpus or cauda epididymidis of Dicer1 c KO mice. [score:4]
This protein participating to the control of sperm forward motility [71], its deregulation in the epididymis by Dicer1 -dependent factors including miR-296 might also have consequences on sperm motility. [score:2]
[1 to 20 of 2 sentences]
18
[+] score: 6
Other miRNAs, including miR-134, miR-145, miR-296 and miR-470 become upregulated during differentiation and have been found to inhibit pluripotency factors such as Oct4, Sox2 and Nanog [10]. [score:6]
[1 to 20 of 1 sentences]
19
[+] score: 5
Zheng Z. Ke X. Wang M. He S. Li Q. Zheng C. Zhang Z. Liu Y. Wang H. Human microRNA hsa-miR-296–5p suppresses enterovirus 71 replication by targeting the viral genome J. Virol. [score:5]
[1 to 20 of 1 sentences]
20
[+] score: 5
Out of 12 miRNA families that were predicted to target the PRKAG1 sense promoter in both human and mouse, nine (miR-718, miR-1224, miR-188, miR-346, miR-296, miR-671, miR-221, miR-1306, miR-506) can form highly stable duplex structures with their target sites (MFE ≤ −30 kcal/mol) in both organisms. [score:5]
[1 to 20 of 1 sentences]
21
[+] score: 5
Another famous study disclosed that growth factor -induced miR-296 contributes significantly to angiogenesis by directly targeting the hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) mRNA leading to decrease levels of HGS and reduce HGS -mediated degradation of the VEGFR2 [30]. [score:5]
[1 to 20 of 1 sentences]
22
[+] score: 5
In fact, this same pattern of regulation was observed for other seven miRNAs (mmu-miR-29c, mmu-miR-296, mmu-miR-130b, mmu-miR-17, mmu-miR-434, mmu-miR-181c, mmu-miR-132), which further confirms the validity of our analysis and suggests miRNA regulation at the gene expression level [48]. [score:5]
[1 to 20 of 1 sentences]
23
[+] score: 5
Others, including let-7f, miR-27b [6], miR-221, and miR-222 [12], have been shown to modulate angiogenesis in vitro and overexpression or inhibition of miR-378 [13], the miR-17-92 cluster [14] and miR-296 [15] affects angiogenesis in mouse engrafted tumors. [score:5]
[1 to 20 of 1 sentences]
24
[+] 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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Six miRNAs showed a trend for a stronger upregulation during the brown adipocyte differentiation - miRPlus_17856, mmu-miR-381, mmu-miR-501-3p, mmu-miR-21*, mmu-miR-296-5p and miRPlus_17832. [score:4]
[1 to 20 of 1 sentences]
25
[+] score: 4
Mir296 and Mir298 are paternal allele-specifically expressed and their transcription in the paternal chromosome depends on the unmethylated allele of the germline DMR located at the Nespas promoter 27 kb away (8). [score:2]
The paternally expressed Nespas RNA (28, 29) extended beyond the Mir296 and Mir298 microRNAs (Supplementary Figure S1C). [score:2]
[1 to 20 of 2 sentences]
26
[+] score: 3
In a more technically advanced study, targeted nanoparticles decorated with a cyclic RGD peptide were used to deliver exogenous miR-296 to tumour vasculature in vivo, resulting in a significant decrease in microvessel formulation 36. [score:3]
[1 to 20 of 1 sentences]
27
[+] score: 2
The upstream regulators of these canonical pathways included CMA1, MKL1, MKL2, NR4A2, and miR-296. [score:2]
[1 to 20 of 1 sentences]
28
[+] score: 2
In triplicate, select miRs were compared against undifferentiated hESCs as well as the 4 endogenous controls, nucleolar RNAs RNU38B and RNU48 (as recommended by the array manufacturer) and the stably expressed miRs, miR-188 and miR-296-5p (as identified in our own experiments) (Figure 1D). [score:2]
[1 to 20 of 1 sentences]
29
[+] score: 2
In addition, miR-296-5p decreased in males and females, and miR-125b-3p showed no changes in male or female brain, consistent with the miRNA arrays. [score:1]
As indicated in Table 1, we examined miR-883b-3p that decreased in males and increased in females, miR-296-5p that decreased in males and females, miR-509-3p that decreased in females (1A). [score:1]
[1 to 20 of 2 sentences]
30
[+] score: 2
miR-296-3p, miR-125a-5p, miR-342 and miR-486 have all been shown to be regulated by retinoic acid (Figure 2; Additional file 4). [score:2]
[1 to 20 of 1 sentences]
31
[+] score: 2
miR-23 and miR-296 seed matches are indicated. [score:1]
Expanding our miRNA site search beyond the 87 miRNA families conserved beyond mammals to the 66 miRNA families conserved only within the mammalian lineage (Figure S9A in Additional file 12), we found that circRNA-ZNF91 had 39 additional sites for miR-296 (Figure  6E). [score:1]
[1 to 20 of 2 sentences]
32
[+] score: 1
Here, 15 miRNAs (miR-let-7e*, miR-15a*, miR-19b-1*, miR-30e*, miR-130b*, miR-149, miR-296-5p, miR-362-5p, miR-378, miR-425, miR-432, miR-484, miR-574-3p, miR-671-5p, and miR-1249) established interactions with 19 mRNAs. [score:1]
[1 to 20 of 1 sentences]
33
[+] score: 1
On the other hand, by RNA ISH we obtained a clear regional hybridization signal for 14 miRNAs that were not detected in a reliable manner by microarray profiling (e. g. miR-188-5p, miR-296-5p, miR-680, miR-681; see database). [score:1]
[1 to 20 of 1 sentences]
34
[+] score: 1
Fu Q miRomics and proteomics reveal a miR-296-3p/PRKCA/FAK/Ras/c-Myc feedback loop modulated by HDGF/DDX5/β-catenin complex in lung adenocarcinomaClin. [score:1]
[1 to 20 of 1 sentences]
35
[+] score: 1
For example, miR-122 is indispensable to replication of the hepatitis C virus (HCV), whereas miR-196 and miR-296 substantially attenuate viral replication [12, 13]. [score:1]
[1 to 20 of 1 sentences]
36
[+] score: 1
These genes have been shown to be silenced by various miRNAs, such as miR-134, miR-145, miR-296 and miR-470 [18]. [score:1]
[1 to 20 of 1 sentences]
37
[+] score: 1
We found two miRs on chr2, namely miR-296 (predicted only twice and located distally on 97.9 cM) and miR-511 (predicted by 6 algorithms and located at 10.5 cM). [score:1]
[1 to 20 of 1 sentences]