sort by

18 publications mentioning rno-mir-92b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-92b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 342
Buechner J. et al revealed that mir-92b expression was downregulated in MYCN ((v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)) repressed SK-N-BE cells [47], In addition, MYCN-regulated mir-92b that could target the 3 [,] UTR sequence of DKK3 (Dickkopf-3), which functions as a tumor suppressor in a range of tumors [48]– [50]. [score:11]
And 22 genes of which that relative fold changes less than 0.5 were considered as potential function targets of miR-92b; (B) Overall, 18 of the 22 3′UTR constructs demonstrated a significant reduction in luciferase activity for 293T cells overexpressing miR-92b (293T-pri-miR-92b), especially C/EBPß; (C) Potential targets could be classified in three aspects: biological process, molecular function and cellular component by using gene function analysis software; (D) Gene ontology analysis of the predicted target genes was performed with Blast2go software. [score:8]
To identify the probable targets involved in differentiation arrested by miR-92b, we performed target prediction based on miRanda algorithm and predicted target cDNA microarray. [score:7]
The significantly increase in G1 phase and decrease in S and G2/M phase could be observed when restoring the C/EBPß expression in miR-92b overexpressed fetal liver cells by transfecting pcDNA-C/EBPß-M. (A) In vivo screening potential targets of miR-92b in EpCAM [+] fetal liver cells by using customized microarray analysis. [score:7]
Gene expression analysis comparing miR-92b overexpressed EpCAM [+] fetal liver cells and control cells was performed with a custom cDNA microarray containing potential target genes of miR-92b. [score:7]
of microarray analysis showed that 7.96% (34/427) of predicted target genes in miR-92b overexpressed EpCAM [+] cells were expressed lower than in counterpart. [score:7]
The data showed that 7.96% (34/427) of predicted target genes in miR-92b overexpressed EpCAM [+] cells were expressed lower than that in the counterpart. [score:7]
The assays showed that luciferase activities in the Luc-C/EBPß, Luc-Gata2, Luc-Foxg1 groups were significantly decreased compared to the luciferase activities of the mutant and control groups; (C) When restoring the C/EBPß expression in miR-92b overexpressed fetal liver cells by transfecting pcDNA-C/EBPß-M constructs, increase of ALB production in miR-92b overexpressed fetal liver cells could be observed, while there are no significant changes about ALB production in mir-92b overexpressed fetal liver cells transfected with pcDNA-C/EBPß, pcDNA-Foxg1, pcDNA-Foxg1-M, pcDNA-Gata2 and pcDNA-Gata2-M, respectively. [score:7]
Within these genes, 22 genes which expression was decreased by <0.5-fold in miR-92b overexpressed EpCAM [+] cells were thought as the most probable target genes of miR-92b (Fig. 7A). [score:7]
we next constructed target gene expression vectors with complete 3′UTR or mutant 3′UTR to identify the major functional target gene involved in differentiation arrest by miR-92b. [score:7]
It suggests that restoration of C/EBPß gene expression in miR-92b overexpressed fetal liver cells reversed the differentiation arrest by miR-92b. [score:5]
According to the mirSVR scores of miRNA/target duplexes are less than 0.1, 3′UTRs on the total of 427 gens were predicted as candidate target sites of miR-92b. [score:5]
This study clarifies that overexpression of miR-92b would result in proliferation increase and differentiation arrest of hepatic progenitors by targeting CCAAT/enhancer binding protein beta (C/EBPß) gene. [score:5]
The functions of many target genes were grouped in the categories of cell differentiation, transcription factor, organ development and regulation of cell proliferation, for choosing the genes involved in differentiation that specially mediated by mir-92b. [score:5]
Luciferase reporter constructs with 3′UTR or mutant 3′UTR of targets and control construct were transfected into miR-92b overexpressed fetal liver cells. [score:5]
These expression vectors were stablely transfected into the miR-92b overexpressed EpCAM [+] fetal liver cells 7 days after induction to differentiate in vivo. [score:5]
Recently, Sengupta et al [44] found that overexpression of miR-92b in human embryonic stem cells would prompt cells progression from G1 phase into S phase by targeting a G1/S checkpoint gene p57, which is not consistent with our results. [score:5]
The significantly increase in G1 phase and decrease in S and G2/M phase could be observed when restoring the C/EBPß expression in miR-92b overexpressed fetal liver cells by transfecting pcDNA-C/EBPß-M. Increasing evidence suggest the presence of LCSCs in many HCC cell lines and primary HCC tissue. [score:5]
The overexpressed miR-92b promoted EpCAM [+] fetal liver cells proliferation and arrested their differentiation by targeting C/EBPß genes. [score:5]
In this study, those miRNA/target duplexes with mirSVR scores less than −0.10 were selected as candidate miR-92b target sites. [score:5]
The EpCAM(+) cells will most probably presented as immature cells, the mir-92b is a inhibitor of cell differentiation, so it is reasonable that the expression level of mir-92b is higher in EpCAM(+) LCSCs. [score:5]
The significantly increase in G1 phase and decrease in S and G2/M phase could be observed when restoring the C/EBPß expression in miR-92b overexpressed fetal liver cells by transfecting pcDNA-C/EBPß-M (Fig. 8D). [score:5]
The significantly increase in G1 phase and decrease in S and G2/M phase could be observed when restoring the C/EBPß expression in miR-92b overexpressed fetal liver cells by transfecting pcDNA-C/EBPß-M. Embryonic 14-day F344 rat fetal liver were used as the cellular source of normal hepatic progenitors, and neoplastic nodules of HCC in F344 rats induced with DEN as the cellular source of LCSCs. [score:5]
Rat target genes potentially regulated by miR-92b were searched from the website (http://www. [score:4]
Figure S2C/EBPβ expression level in the miR-92b overexpressed EpCAM [+] cells had significantly decreased compared to that in control cells. [score:4]
miR-92b was downregulated in EpCAM [+] fetal liver cells. [score:4]
miR-92b is upregulated in human HCC and associated with histological differentiation. [score:4]
To assess the direct functional target of miR-92b involved in differentiation arrest of fetal liver cells, we initially investigated the binding sites of miR-92b in 3′UTR of three pinpointed target genes (C/EBPß, Gata2, Foxg1). [score:4]
C/EBPß is a direct functional target of miR-92b. [score:4]
In addition, we confirmed that results that the C/EBPß is direct targets of miR-92b by western bolt (Fig. S2). [score:4]
miR-92b was the most upregulated miRNA in our profiling studies, and we selected it for further analysis. [score:4]
It suggests that the C/EBPß, Gata2 and Foxg1 receptors are direct targets of miR-92b in fetal liver cells. [score:4]
miR-92b was downregulated in EpCAM [+] fetal liver cellsEmbryonic 14-day F344 rat fetal liver were used as the cellular source of normal hepatic progenitors, and neoplastic nodules of HCC in F344 rats induced with DEN as the cellular source of LCSCs. [score:4]
miR-92b was the most up-regulated miRNA in this profiling study, with 3.56±1.02 fold changes after normalization (q = 0.000, FDR = 0.036). [score:4]
However, further studies involving analysis of mechanism of miR-92b upregulation in liver cancer stem cells are required. [score:4]
Whereas, only small satellite clusters of GFP positive cells with the small oval cell morphology embedded in the region of the hepatic lobule closed to portal area could be observed in the sections transplanted with miR-92b overexpressed group (Fig. 6B). [score:3]
Final analysis of gene function classification pinpointed three transcription factor genes are directly involved in the differentiation regulated by miR-92b. [score:3]
The current study addition to differentiation arrest, proliferation was significantly increased in the miR-92b overexpressed EpCAM [+] fetal liver cells. [score:3]
The 3′UTR of the C/EBPß, Gata2 and Foxg1 genes contain putative target sites with the position of seed sequences as indicated; (B) Fetal liver cells transfected with pri-miR-92b and a luciferanse reporter containing a fragment of the 3′UTR harboring either the miR-92b binding site (Luc-C/EBPß, Luc-Gata2, Luc-Foxg1) or a mutant (Luc-C/EBPß-M, Luc-Gata2-M, Luc-Foxg1-M). [score:3]
Histopathogical examination showed that the degree of repair was better in livers of the rats injected with control group than the rats injected with miR-92b overexpressed group (Fig. 6A). [score:3]
The ultrastructure was more preserved in control cells comparing to the miR-92b overexpressed cells. [score:3]
Next, the expression pattern of miR-92b was correlated with clinicopathological parameters of HCC. [score:3]
In addition, miR-92b overexpressed group and control group were orthotopically transplanted into the livers of nude mice. [score:3]
showed that overexpression of miR-92b in EpCAM [+] fetal liver cells would result in the decrease in G [1] phase and significantly increase in S and G [2]/M phase. [score:3]
0068004.g002 Figure 2(A) miR-92b was differentially expressed between HCC and the corresponding nontumoral liver tissues. [score:3]
0068004.g007 Figure 7(A) In vivo screening potential targets of miR-92b in EpCAM [+] fetal liver cells by using customized microarray analysis. [score:3]
The livers transplanted with miR-92b overexpressed cells had a typical variegated appearance with extensive lesion. [score:3]
The relationships between the miR-92b and other mRNA expressions were analyzed by correlation coefficients and linear regression analysis. [score:3]
ALB and urea secretion had been increased from day 7 and 9 respectively reaching maximal values on day 14 in the medium of control group, which were dramatically higher than that in the medium of miR-92b overexpressed group (P<0.05, Fig. 5C). [score:3]
On other hands, the large, round, hyperchromatic unclei, poor number of cellular organelles, nonpolarity, with the increased nuclear/cytoplasm ratio were observed in the miR-92b overexpressed cells as a phenotype in the liver progenitor-like cells (Fig. 4). [score:3]
showed the rescue effects of C/EBPß in miR92b overexpressed fetal liver cells. [score:3]
In addition, control group was positive for PAS staining indicating the glycogen storages, while the differentiated miR-92b overexpressed group was negative for PAS staining (Fig. 5B). [score:3]
Cell cycle analysis showed that overexpression of miR-92b in EpCAM [+] fetal liver cells would result in the decrease in G [1] phase and significantly increase in S and G [2]/M phase. [score:3]
In addition, overexpression of miR-92b in EpCAM+ fetal liver cells would result in the significantly G2/M phase (13.5%±2.4% vs 11.4%±2.1%, P<0.05). [score:3]
miR-92b expression in clinical HCC samples. [score:3]
And we can accordingly predict that C/EBPß might also be one of the key target genes of the miR92b in human species, which needs further study. [score:3]
Phase-contrast microscopy revealed the miR-92b overexpressed cells were similar to immature cells, at intermediate stage from hepatic progenitor to mature hepatocyte. [score:3]
These miR-92b overexpressed immature cells were small, mononuclear, round or oval-shaped and usually arranged in cobblestone-like appearance. [score:3]
Prediction and identification of miR-92b targets. [score:3]
However, most of the miR-92b overexpressed cells were similar to immature cells and still at the intermediate stage from hepatic progenitor to mature hepatocyte. [score:3]
The relative expression of miR-92b was significantly associated with a degree of differentiation (P<0.05, Table 2). [score:3]
Further, we studied the hepatocyte-specific biochemical functions to prove the hepatocyte differentiation arrest caused by overexpression of miR-92b. [score:3]
Large clusters of red fluorescence -positive cells with hepatocyte morphology were observed in the control group, and only small satellite clusters of GFP positive cells with the small oval cell morphology could be observed in the miR-92b overexpressed group. [score:3]
Predicting functional target genes of miR-92b. [score:3]
Ectopic miR-92b overexpressed EpCAM [+] fetal liver cells were established as follows: Firstly, lentiviral infection was performed on the primary cultures of fetal liver cells. [score:3]
The percentage of miR-92b overexpressed and control groups in the G [0]/G [1] phase respectively were 67.2%±2.2% and 84.3%±3.1% (P<0.05). [score:3]
Finally, the miR-92b overexpressed EpCAM [+] cells could be enriched by performing FACS to the transfectants for further study. [score:3]
Control cells and mir-92b overexpressed cells were independently washed with PBS in the dark and resuspended in 2 ml staining solution to label the cell membrane with red fluorescence or GFP, respectively. [score:3]
Then customized microarray analysis was performed on miR-92b overexpressed and control groups enriched by FACS. [score:3]
Under microscopic observation, the liver section transplanted with miR-92b overexpressed cells showed that portal area were filled with plenty of small oval immature cells, these cells extensively invaded into the adjacent lobule and destroy associated structure of lobules. [score:3]
It suggests that single overexpression of miR-92b in hepatic stem cells would result in abnormal proliferation (data not shown). [score:3]
Moreover, expression of miR-92b was positively associated with AFP mRNA (r = 0.554, P<0.05, Fig. 2B). [score:3]
However, AFP mRNA level in the miR-92b overexpressed group were significantly increased in comparison with the control group on 96 h and 2w after differentiation induction (P<0.05 and <0.05, respectively). [score:3]
The effect of miR-92b overexpression on repopulation capacity of EpCAM [+] fetal liver cells was studied with in vivo differentiation assay. [score:2]
In vivo differentiation assay of the effect of miR-92b overexpression on liver repopulation capacity of EpCAM [+] fetal liver cells. [score:2]
miR-92b regulates cell proliferation and differentiation of EpCAM [+] fetal liver cells. [score:2]
The significant maturation arrest was found in EpCAM [+] cells isolated from the miR-92b overexpressed fetal liver cells detected by both in vitro and in vivo differentiation assay. [score:2]
Among the 152 HCC clinical samples, relative expression of miR-92b in HCC was significantly higher compared to nontumoral liver tissues (6.25±2.08 vs 2.96±1.23, P<0.01. [score:2]
We uniquely demonstrated that percentage of miR-92b overexpressed group in S and G2/M phase significantly increased compared with control group. [score:2]
This phenomenon is similar with our result of in vivo differentiation assay, which indicates that C/EBPß may be a critical downstream target of miR-92b. [score:2]
If miR-92b expression in tumor tissues was 2 times higher than in the nontumoral liver tissues, it was considered as a “high” result. [score:2]
Our previous report also revealed that the relative expression levels of miR-92b, miR-21, miR-34c, miR-10b, and let-7i in EpCAM [+] liver cancer cells compared to fetal liver cells were increased (P<0.05). [score:2]
miR-92b regulated the proliferation of EpCAM [+] fetal liver cells. [score:2]
0068004.g006 Figure 6 In vivo differentiation assay of the effect of miR-92b overexpression on liver repopulation capacity of EpCAM [+] fetal liver cells. [score:2]
A series of biological function assays were performed on miR-92b overexpressed group or control group to explore the effect of miR-92b on primary cultures of hepatic progenitors. [score:2]
Compared with the control group, the miR-92b overexpressed group had significantly decreased ALB mRNA levels (P<0.05). [score:2]
The control image was showing the mature degree and apoptosis of control cells compared to the mir-92b overexpressed cells, especially the cells in the white lines. [score:2]
Effects of miR-92b on the hepatic differentiation and maturation of EpCAM [+] fetal liver cells. [score:1]
Firstly, we assessed the effect of miR-92b on modulation and proliferation of hepatic progenitors (Fig. 3). [score:1]
Whether p57 gene also involved in the changes of cell cycle caused by overexpression of miR-92b in the hepatic progenitors needs further investigation. [score:1]
Furthermore, gain-of-function studies were performed in vitro and in vivo to determine the role of miR-92b in the hepatic progenitors. [score:1]
Our survey detected increases of miR-92b during hepatocarcinogenesis. [score:1]
In our later study, we are planning to combine the miR-92b with miR-200a or miR-21 to search for the mechanisms of malignant transformation. [score:1]
0068004.g004 Figure 4Effects of miR-92b on the hepatic differentiation and maturation of EpCAM [+] fetal liver cells. [score:1]
0068004.g005 Figure 5Effects of miR-92b on the differentiation arrest of EpCAM [+] fetal liver cells. [score:1]
Our results indicated that miR-92b played the role most probably by influencing C/EBPß. [score:1]
Our data showed that the mir-92b might contribute to the malignant transformation of the liver stem cells, which may be a new valuable marker of HCC, and the analogy between the already confirmed miRNAs such as antioncogene mir-200a [45] or Oncogene mir-21 [46]. [score:1]
The first important finding our current study is the functional role of miR-92b involved in the differentiation of hepatic progenitors. [score:1]
Effects of miR-92b on the differentiation arrest of EpCAM [+] fetal liver cells. [score:1]
[1 to 20 of 99 sentences]
2
[+] score: 39
The mRNA encoding the cyclin dependent kinase inhibitor 1c (Cdkn1c) was up-regulated 3-fold in E13 ENPs and is predicted to be targeted by three miRNAs that were down-regulated: miR-92, miR-222, and miR-363-3p. [score:11]
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
Focusing on the down-regulated miRNAs that had a significant negative correlation in Figure 6, we performed network analysis and identified miR-92, miR-183, miR-222 and miR-291-3p as predicted to target multiple TFs that were up-regulated in E13 ENPs (Figure 8). [score:9]
Additional support for this hypothesis was provided by the miRNA-TF mRNA network analysis in Figure 8. We found four down-regulated miRNAs (miR-92, miR-183, miR-222 and miR-291-3p) that were predicted to target multiple TFs, which were up-regulated in E13 ENPs. [score:9]
[1 to 20 of 4 sentences]
3
[+] score: 23
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
In the ceRNA network, lncRNA TCONS_00097976 connected with miR-92b-3p and miR-92b-3p target gene Stat3. [score:3]
Some of the differentially expressed miRNAs were previously reported (miR-223, miR-129, and miR-92) [4, 5], which support our results. [score:3]
LncRNA TCONS_00097976 is connected to angiogenesis-related miR-92b-3p and angiogenesis-related genes Esm1, Angptl2, and Stat3, which have been reported differently expressed in ischemic stroke [25, 26]. [score:3]
Thus, TCONS_00097976 would compete with miR-92b-3p to regulate these angiogenesis genes during focal ischemia. [score:2]
miR-92 was previously reported as regulator of angiogenesis and cardiac ischemic/reperfusion injury [25, 39]. [score:2]
Thus, TCONS_00097976-miR-92b-3p-Stat3 would be ceRNA mediated ischemia response networks which participated in the regulation of angiogenesis after ischemic stroke. [score:2]
Intriguingly, miR-129-2-3p and miR-92b-3p were contained in the ceRNA networks. [score:1]
[1 to 20 of 8 sentences]
4
[+] score: 13
A recent study reported that the long non-coding RNA XIST functioned as a competing endogenous RNA to modulate EZH2 expression by mopping up miR-101 in gastric cancer [11], and that XIST is targeted and regulated by miR-92b in Hepatocellular carcinoma (HCC). [score:6]
In hepatocellular carcinoma (HCC), it has been shown that the knockdown of XIST by si -RNA (si-XIST) could affect the proliferation and metastasis of tumor cells by regulating the expression of miR-92b [17]. [score:5]
Zhuang L. K. Yang Y. T. Ma X. Han B. Wang Z. S. Zhao Q. Y. Wu L. Q. Qu Z. Q. MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XISTCell Death Dis. [score:2]
[1 to 20 of 3 sentences]
5
[+] score: 8
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
[1 to 20 of 2 sentences]
6
[+] score: 7
MiR-92, another member of the cluster, has been shown to regulate myocardial angiogenesis through targets distinct from those of miR20a, including integrin subunit alpha5 [14]. [score:4]
Note relatively higher expression of 3′ members of the cluster, miR-20a, miR-19b, and miR-92. [score:3]
[1 to 20 of 2 sentences]
7
[+] score: 6
The hypoxia-exposed BM-MSC-conditioned media significantly reduced apoptosis in cardiomyocytes and suppressed the hypoxia -induced up-regulation of miRNA-23a and miRNA-92. [score:6]
[1 to 20 of 1 sentences]
8
[+] score: 6
In this study, miR-92b (one member of the miR-17-92 family) was highly expressed in SP-HCCs. [score:3]
In this study, miR-10b, miR-21 and miR-92b were frequently over-expressed. [score:3]
[1 to 20 of 2 sentences]
9
[+] score: 5
While the reduction in expression of miR-17-5p, miR-18a, miR-20a, and miR-92 were well coordinated in transdifferentiation, the expression of miR-19a was not concordant with its neighboring microRNA genes. [score:5]
[1 to 20 of 1 sentences]
10
[+] score: 4
The upregulated miRNAs in the colon tissues of UC rats changed by HM were miR-149-5p, miR-351-5p, let-7d-5p, miR-98-5p, let-7a-5p, miR-3559-5p, let-7f-1-3p, miR-3596b, miR-224-5p, miR-411-3p, miR-184, miR-26b-3p, and miR-92b-3p. [score:4]
[1 to 20 of 1 sentences]
11
[+] score: 2
control Function rno-miR-653-3p 37.56097561 Unknown rno-miR-3594-3p 9.31358885 Unknown rno-miR-483-3p 8.414634146 Anti-apoptotic oncogene, cardiovascular inflammation and remo delling rno-miR-92b-5p 8.096126255 Heart development and atrial fibrillation rno-miR-377-5p 4.84735544 Atrial fibrillation and structural remo delling rno-miR-341 4.764878049 Atrial fibrillation and TGF-β/Smad2/3 pathway rno-miR-21-3p 4.637785208 Cell proliferation and invasion. [score:2]
[1 to 20 of 1 sentences]
12
[+] score: 2
The expression patterns of some miRNAs observed in our study are consistent with what were observed in previous studies by using the blot-array and Northern blot assays, i. e. miR-125b, miR-9, and miR-181a [6], as well as miR-29a, miR-138 and miR-92 [53]. [score:2]
[1 to 20 of 1 sentences]
13
[+] score: 2
Other miRs which were more abundant in CDC-EVs vs MSC-EVs included miR-124, miR-210, miR-92 and miR-320. [score:1]
Another miR similarly abundant in human- and rat-CDC-EVs, and significantly higher compared with MSC-EVs, was miR-92, a member of the miR-17-92 cluster, and an important regulator of cancer and aging [46]. [score:1]
[1 to 20 of 2 sentences]
14
[+] score: 1
Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
[1 to 20 of 1 sentences]
15
[+] score: 1
On the other hand, a few miRs have been found to promote apoptosis of myocardiocytes, such as miR-26 [29], miR-34 [30], and miR-92 [31]. [score:1]
[1 to 20 of 1 sentences]
16
[+] score: 1
Additionally, four miRNAs (miR-138, miR-146b, miR-301a, and miR-92b) were common between our data and those of Kan et al. in human temporal lobe epilepsy [22]. [score:1]
[1 to 20 of 1 sentences]
17
[+] score: 1
Other miRNAs from this paper: cel-let-7, cel-lin-4, 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-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, 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-29a, mmu-mir-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, 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-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-1, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, hsa-mir-421, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The probes used were: EAM119 (miR-29b), EAM125 (miR-138), EAM224 (miR-17-5p), EAM234 (miR-199a), EAM131 (miR-92), EAM109 (miR-7), EAM150 (miR-9) and EAM103 (miR-124a). [score:1]
[1 to 20 of 1 sentences]
18
[+] score: 1
MiR-17-5p belongs to the miR-17~92 cluster, located on the human chromosome 13q31, and is a prototypical example of a polycistronic miRNA gene encoding six miRNAs (miR-17-5p, miR-18, miR-19a, miR-19b, miR-20 and miR-92). [score:1]
[1 to 20 of 1 sentences]