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80 publications mentioning mmu-mir-429

Open access articles that are associated with the species Mus musculus and mention the gene name mir-429. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 97
In order to understand how IGF-1 suppresses miR-429 in UUO mice, we used specific inhibitors of IGF-1 downstream signaling in IGF-1 -treated renal epithelial cells in vitro and examined their effects on Bcl-2. While no effects of inhibition of PI3k/Akt and JNK signaling pathways were detected in IGF-1 -treated renal epithelial cells, inhibition of ERK1/2 signaling pathway by ERK/MAPK-p42/p44 inhibitor PD98059 (Fig. 5A) significantly abolished the effects of IGF-1 on miR-429 (Fig. 5B) and Bcl-2 activation (Fig. 5C,D). [score:11]
IGF-1 suppresses miR-429 that targets 3′-UTR of Bcl-2 mRNA to inhibit its translation in renal epithelial cells. [score:9]
In order to figure out whether the binding of miR-429 to Bcl-2 mRNA in renal epithelial cells is functional, we either overexpressed miR-429, or inhibited miR-429 in the purified renal epithelial cells, by transfecting the cells with plasmids carrying either a miR-429 -mimic (miR-429), or a miR-429 antisense (as-miR-429). [score:5]
IGF-1 may protect tubular epithelial cells against renal injury via ERK/MAPK signaling pathway -dependent suppression of miR-429, and miR-429 inhibits Bcl-2 -dependent anti-apoptosis. [score:5]
Specifically, miR-429 has been shown to suppress Bcl-2 protein translation in gastric cancer cells 25 and endothelial cells 24. [score:5]
Hence, targeting suppression of Bcl-2 by miR-429 was analyzed and confirmed. [score:5]
The overexpression or inhibition of miR-429 in renal epithelial cells was confirmed by RT-qPCR (Fig. 4C). [score:5]
Our data showed that Bcl-2 expression in UUO is significantly higher than in sham group, while miR-429 is highly expressed in UUO than in sham. [score:5]
The overexpression or inhibition of miR-429 in renal epithelial cells was confirmed by RT-qPCR. [score:5]
The luciferase activities were quantified in these cells, suggesting that the binding of miR-429 to 3′-UTR of Bcl-2 mRNA results in suppression of Bcl-2 protein translation in renal epithelial cells (Fig. 4D). [score:5]
These data suggest that miR-429 indeed inhibits Bcl-2 protein translation in renal epithelial cells. [score:5]
Hence, our data suggest that IGF-1 may protect tubular epithelial cells against renal injury via ERK/MAPK signaling pathway -dependent suppression of miR-429, and miR-429 inhibits Bcl-2 -dependent anti-apoptosis (Fig. 6). [score:5]
However, endogenous miR-429 expression may be a part of the negative regulatory loop of the Bcl-2 in kidney epithelial cells under stress. [score:4]
Target sequences for Bcl-2 3′-UTR and Bcl-2 3′-UTR with a site mutation at miR-429 binding site (Bcl-2 3′-UTR mut) were purchased from Creative Biogene (Shirley, NY, USA). [score:4]
IGF-1 suppresses miR-429 through ERK1/2 signaling pathway. [score:3]
MiR-429 -expressing, antisense of miR-429 (as-miR-429) and control null plasmids were all purchased from RiboBio Co. [score:3]
Here, by sequence matching using bioinformatics analyses, we found quite a few of candidate miRNAs that target Bcl-2, including miR-429, miR-30, miR-22, miR-25, miR-32, miR-92, miR-363, miR-367, miR-99, miR-27, miR-128, etc. [score:3]
To the best of our knowledge, the current study was the first report showing that miR-429 is regulated by IGF-1, and in an ERK/MAPK-p42/p44-signaling pathway -dependent manner. [score:2]
Purified renal epithelial cells were seeded in 24-well plates for 24 hours, after which they were co -transfected with 1 μg of Luciferase-reporter plasmids and miR-429 -modified plasmids. [score:1]
When the cells are not insulted, their Bcl-2 levels are low and miR-429 levels are also low. [score:1]
MiR-429 -modified renal epithelial cells were then transfected with 1 μg of Bcl-2 3′-UTR luciferase-reporter plasmid or with 1 μg of Bcl-2 3′-UTR luciferase-reporter plasmid with a site mutation between 440 [th] to 447 [th] base site. [score:1]
When Bcl-2 is activated after UUO, the miR-429 may be activated to counteract the increases in Bcl-2. Moreover, when IGF-1 is administrated, it may decrease miR-429 levels, resulting in loss of control of increases in Bcl-2. However, since miR-429 is not responsible for the control of Bcl-2 levels in UUO vs sham, and the Bcl-2 level changes in UUO also appeared to posttranscriptional, we think that another posttranscriptional control of Bcl-2 levels by factors other than miR-429 may be present in kidney epithelial cells after UUO, possibly the control of protein degradation of Bcl-2. Future studies may address these questions. [score:1]
We found that Bcl-2 mRNA was not altered by miR-429 modification (Fig. 4E). [score:1]
Specifically, we found that miR-429 had a binding site at the 3′-UTR of Bcl-2 mRNA ranged from 440 [th] to 447 [th] base site (Fig. 4A). [score:1]
Moreover, the levels of miR-429 in renal epithelial cells were significantly decreased In IGF-1 -treated mice that received UUO (Fig. 4B). [score:1]
However, Bcl-2 protein was significantly decreased in miR-429 -transfected renal epithelial cells, and significantly increased in as-miR-429 -transfected renal epithelial cells (Fig. 4F). [score:1]
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2
[+] score: 69
Overexpression of miR-429 inhibits invasion and promotes apoptosis in esophageal carcinoma cells by targeting Bcl-2 and SP1 (19). [score:7]
org, miRDB, RNA22-HSA and PITA) were used to predict the candidate targets of miR-429, ZEB1, ZEB2, WIPF1, MARCKS, TRIM33, WASF3, CRKL, WAPAL and NTRK2 were predicted as candidate targets of miR-429 (Table I). [score:5]
miR-429 mediates inhibitory function by targeting multiple genes. [score:5]
Besides in breast cancer, overexpression of miR-429 suppressed invasion and metastasis of colorectal carcinoma and ovarian cancer cells, respectively (20, 31). [score:5]
To gain insight into the roles of miR-429 inhibiting bone metastasis of MDA-MB-231 cells, several computational algorithms (including TargetScan, DIANA-microT, microRNA. [score:5]
miR-429 inhibits cells invasion by targeting Onecut2 in colorectal carcinoma (20). [score:5]
In the present study, we showed that downregulation of miR-429 could promote bone metastasis of breast cancer, which is in line with previously reported results in several types of cancers. [score:4]
For example, Onecut2 was proved to be one bona fide target of miR-429 in colon cancer (20). [score:3]
Besides ZEB1, several candidate targets of miR-429 were also identified essential for invasion and metastasis in cancer mo dels. [score:3]
ZEB1 is the most well studied target of miR-429, since this transcription factor is an important EMT inducer (33). [score:3]
miR-429 suppresses invasion of 231-B cells in vitro. [score:3]
We noted that miR-429 expression was significantly lower in 231-B cells than that of 231-P cells (Fig. 3B). [score:3]
Collectively, miR-429 negatively modulated several key invasion and metastasis inducers to suppress motility of breast cancer cells. [score:3]
Previous reports showed that miR-429 could inhibit migration and metastasis of several types of cancers. [score:3]
Especially, we focus on the biological function of miR-429 through its target genes ZEB1 and CRKL. [score:3]
Then, we combined the in silico analysis of miR-429 targets and global transcriptional profile (Fig. 5B). [score:3]
Taken together, miR-429 probably regulated bone metastasis of breast cancer cells in a negative manner. [score:2]
We transfected miR-429 mimics into 231-B cells, which was verified by real-time PCR assay (Fig. 4A), and found that overexpression of miR-429 could dramatically reduce the migration and invasiveness of 231-B cells (Fig. 4B). [score:2]
miR-429 is a member of the miR-200 family, four members of this family have been found to play important roles in the regulation of EMT in various types of tumors (29). [score:2]
[1 to 20 of 19 sentences]
3
[+] score: 54
For example, Hlf was targeted by mmu-miR-18b-5p, mmu-miR-429-3p and mmu-miR-291a-3p; Cnot6 and Zfp91 were targeted by mmu-miR-206-3p and mmu-miR-291a-3p; Rbfox2 was targeted by mmu-miR-429-3p and mmu-miR-449c-5p; Aebp2 was targeted by mmu-miR-125a-3p, mmu-miR-223-3p and mmu-miR-496-3p; Nfya was targeted by mmu-miR-199a-5p, mmu-miR-216b-5p and mmu-miR-671-5p; Nucks1 was targeted by mmu-miR-142-3p, mmu-miR-146a-5p and mmu-miR-223-3p; Notch2 was targeted by mmu-miR-146a-5p and indirectly via Ascl1 by mmu-miR-1903. [score:16]
Mmu-miR-145-5p was strongly down-regulated in myopic retina (FC = -10.5, p = 8.87 × 10 [−09]) and targeted 25 mRNAs, while mmu-miR-429-3p was strongly up-regulated in myopic retina (FC = 7.8, p = 2.05 × 10 [−03]) and targeted 17 mRNAs (Table 2). [score:11]
Although the majority of the differentially expressed miRNAs originated from different miRNA clusters, mmu-miR-429-3p and mmu-miR-200a-5p belonged to the same cluster (MID < 5 kb) on chromosome 4 and were both up-regulated in myopic retina, while mmu-miR-145-5p and mmu-miR-143-3p localized within the same cluster (MID < 5 kb) on chromosome 18 and were both down-regulated in myopic retina (Table 1) [68]. [score:9]
For example, mmu-miR-145-5p, which was strongly down-regulated in myopic retina (FC = -10.5, p = 8.87 × 10 [−09]), targeted 25 mRNAs (the largest number among all 21 miRNAs) (Table 2); while mmu-miR-429-3p (FC = 7.8, p = 2.05 × 10 [−03]), mmu-miR-143-3p (FC = -2.0, p = 1.43 × 10 [−03]), mmu-miR-223-3p (FC = -2.7, p = 4.84 × 10 [−04]) and mmu-miR-146a-5p (FC = -3.2, p = 2.70 × 10 [−05]) targeted 17, 17, 16 and 14 mRNAs respectively. [score:8]
For example, miR-200a, miR-429 and miR-141 were shown to play important roles in neurogenesis, epithelial-to-mesenchymal transition and Notch signaling [73, 75– 84], miR-214 was found to be overexpressed in fetal sclera versus adult sclera and shown to play important role in brain and retina development and function [36, 85– 89], miR-18b, miR-21, miR-101a, miR-200a and miR-429 were found to be involved in stem cell function and differentiation [90– 100], miR-1306 negatively regulated Alzheimer’s disease gene ADAM10 [101]. [score:7]
Interestingly, mmu-miR-145-5p and mmu-miR-429-3p (mmu-miR-200b-3p cluster), which formed a common core of all pathways, were among the most differential miRNAs and targeted the largest number of mRNAs. [score:3]
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4
[+] score: 41
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-200a, mmu-mir-200c
In this study, we found that miR-200a, miR-200b and miR-429 were upregulated in DMPCs, whereas the expression of miR-200c and miR-141 were not affected (Fig. 1). [score:6]
Notably, the three miR-200a/200b/429 are all located on chromosome 4, which indicates a potential key role of the three members on chromosome 4 in podocyte differentiation, but not the other two members (miR-200c and miR-141) on chromosome 6. Thus, a negative control or miR-200a, miR-200b and miR-429 inhibitors were all co -transfected together into DMPCs for 48 h. We found that restraint of miR-200 family significantly inhibited podocyte differentiation (Figs 2 and 3). [score:5]
To confirm the biological function of miR-200 family in podocyte differentiation, we examined cell cycle distribution after a simultaneous inhibition of the expression of miR-200a, miR-200b and miR-429. [score:5]
In the present study, we demonstrated that miR-200a, miR-200b and miR-429 are significantly up-regulated during the podocyte differentiation. [score:4]
Compared with DMPC group (76.3 ± 0.5%), a significant decrease of cells in the G0/G1 phase of cell cycle was observed following miR-200a, miR-200b and miR-429 co -inhibition (miR-200a/200b/429 inhibitors-DMPC group; 63.3 ± 4.5%, P < 0.001)(Fig. 2a). [score:4]
showed that miR-200a (P < 0.01), miR-200b (P < 0.05) and miR-429 (P < 0.05) significantly down-regulated the luciferase activity of RSAD2 construct (Fig. 5a), whereas luciferase activity was not generated from the mutant construct (Fig. 5b). [score:4]
Upregulation of miR-200a, miR-200b and miR-429 during the differentiation of podocytes. [score:4]
The miRNA microarray showed that miR-200a, miR-200b and miR-429 expressions were significantly increased in differentiated podocytes (Fig. 1a). [score:3]
Total RNA isolation and qPCR for detecting miR-200a, miR-200b, miR-429 and RSAD2 mRNA expression were carried out by the following procedures. [score:3]
Further real-time quantitative PCR (qPCR) assay showed that miR-200a (1996 ± 470, P < 0.01), miR-200b (543 ± 92, P < 0.01) and miR-429 (463 ± 74, P < 0.01) expressions were significantly increased in differentiated podocytes (Fig. 1b). [score:2]
The miR-200a, miR-200b and miR-429 mimics and vectors containing the 3′-UTR of RSAD2 were transiently transfected into HEK293 cells. [score:1]
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5
[+] score: 32
Knocking down miR-200b in our mice resulted in down-regulation of mature miR-200a and miR-429. [score:5]
Although miR-200a and miR-429 were expressed lower in miR-200b [−/−] lungs, their expression was not undetectable like miR-200b. [score:5]
Based on our studies, we cannot exclude that downregulation of miR-200a and miR-429 contributed to the observed lung phenotype in miR-200b deficient mice. [score:4]
miR-200a and miR-429 were significantly downregulated, but no changes were observed in abundance of miR-200c and miR-141 ** P < 0.01, Student’s t-test, Data represent mean ± SEM of at least four independent experiments. [score:4]
However, it is unclear at this point what the influence of downregulation of miR-200a and miR-429 on the lung phenotype of miR-200b deficient mice is. [score:4]
In contrast to miR-200b/miR-429 [−/−] mice reported by others [23], our miR-200b [−/−] mice carried a lacZ-reporter gene that we exploited to localize miR-200b promoter activity during development (Fig.   1c). [score:2]
MiR-200b belongs to the miR-200 family (miR-141, miR-429, miR-200a, miR-200b and miR-200c) and regulates epithelial-to-mesenchymal transition (EMT) in cancer and organ fibrosis 17– 20. [score:2]
We showed that mature microRNAs transcribed in the same cluster - miR-200a and miR-429 - were still expressed, albeit lower compared to miR-200b [+/+] lungs (Fig.   1f, Supplementary Fig. 5). [score:2]
Mature microRNAs transcribed in the same cluster–miR-200a and miR-429–were still expressed, albeit lower compared to miR-200b [+/+] lungs (wt). [score:2]
We also observed lower miR-200a and miR-429 in kidney tissues of miR-200b [−/−] mice (Supplementary Fig. 6). [score:1]
Like what we observed in fetal lungs, adult miR-200b [−/−] lungs had lower miR-200ba and miR-429 abundance, but no changes in miR-200c and miR-141 abundance (Supplementary Fig. 5). [score:1]
[1 to 20 of 11 sentences]
6
[+] score: 31
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-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, 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-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, 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-96, 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-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
We found eight miRs differentially expressed, six down-regulated (miR-9, miR-141, miR-200a, miR-200b, miR-429 and miR-376a) and two up-regulated (miR-450a-5p and miR130b*) in the Dlx5 [−/−] OE (Fig.  1a). [score:9]
Thus, Dlx5 is likely to regulate the expression of miR-9.3 directly, and the expression of miR-200a/ b/ miR-429 indirectly. [score:8]
We observed a reduction of miR-9, miR-141 and miR-429 signal in the Dlx5 [−/−] OE, compared to the WT (Fig.  1c), while hybridization with two positive controls, Sp8 (expressed in the OE) and Sox5 (expressed in chondrogenic condensations), yielded an equivalent positive signal in both genotypes, indicating adequate RNA preservation. [score:4]
Alternatively the expression of miR-200a/ b/ miR-429 could require additional transcription (co)factors not present in these cells. [score:3]
miR-200a, miR-200b, miR-141 and miR-429 share the same seed sequence and likely target the same mRNAs; for this reason they are grouped in a single miR class (named miR-200-class). [score:3]
Since miR-200a, miR-200b, miR-141 and miR-429 share very similar seed sequences (Suppl. [score:1]
As a further confirmation, we carried out in situ hybridization on sections of WT and Dlx5 [−/−] embryonic OE, at the age E12.5, to detect miR-9, miR-141 and miR-429, using specific mouse DIG -labelled probes. [score:1]
To test whether the DLX5 protein physically occupies the Dlx5 sites near the miR-9.3 and miR-200a/ b/ miR-429 loci, Chromatin Immuno-Precipitation (ChIP) analysis on these sites was performed. [score:1]
Recently, miR-200b and miR-429 have been linked to pituitary endocrine functions controlling ovulation and fertility in female mice (Hasuwa et al., 2013). [score:1]
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7
[+] score: 31
Moreover, out of 12 miRNAs targeting SREBP-1c and/or HMGCR, five were significantly up-regulated in liver of leptin -treated chicks, including gga-miR-200b and gga-miR-429, which target both SREBP-1c and HMGCR. [score:8]
We observed the uncoupling of HMGCR mRNA (up-regulated) and protein (unchanged) in the liver of leptin -treated chicks, which coincided with significantly increased expression of gga-miR-200a gga-miR-200b and gga-miR-429 that were predicted to target the chicken HMGCR gene. [score:8]
Among the five miRNAs predicted to target SREBP-1c, gga-miR-99a, gga-miR-100, gga-miR-200b and gga-miR-429 were found to be significantly (P < 0.05) up-regulated in the liver of leptin -treated chickens. [score:6]
Among the nine miRNAs predicted to target HMGCR, the expression of gga-miR-200a, gga-miR-200b and gga-miR-429 was significantly increased (P < 0.05). [score:5]
It is worth noting that gga-miR-200b and gga-miR-429 were predicted to target both SREBP-1c and HMGCR (Table 5). [score:3]
It is noteworthy that gga-miR-99a and gga-miR-100 belong to the miRNA gene family of miR-99, while the remaining three miRNAs, gga-miR-200a, gga-miR-200b and gga-miR-429, belong to the miRNA gene family of miR-8, located in the same miRNA cluster. [score:1]
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8
[+] score: 25
The TargetScan5.0 algorithm identified the zinc finger E-box binding homeobox 2 (Zeb2/SIP1/ZFXH1B) gene as the highest likelihood target gene of the miR-200 family with 6 potential miR-429/miR-200b/miR-200c binding sites and an additional 3 potential miR-141/miR-200a binding sites in its 3′UTR. [score:5]
The cells incapable of colonization had very low to undetectable expression of all miR-200 family members, while 4T1 cells expressed miR-429, miR-200b and miR-200c. [score:5]
The members of the miR-200 family of miRNAs (miR-200b, miR-200c and miR-429) were highly expressed in 4T1 cells but undetectable in 4TO7 cells. [score:3]
In fact, expression of miR-429, miR-200b and miR-200c was elevated in the highly metastatic 4T1 cells but absent from 4TO7 cells, which can perform all of the steps leading up to the establishment of lung metastases except establishing the secondary tumor. [score:3]
Although highly homologous, the miR-200 family members (miR-141, miR-429, miR-200a, miR-200b and miR-200c) can be divided into two functional groups based on their seed sequences, nucleotides 2 to 7 of the miRNA, which play an important role in target recognition. [score:3]
In addition, they are encoded from 2 gene clusters in mice - miR-200c and miR-141 on chromosome 6 and miR-200b, miR-200a and miR-429 on chromosome 4. In agreement with recent papers [30]– [37], we found that the miR-200 family members target the transcriptional repressor Zeb2. [score:3]
Expression of some members of the miR-200 family of miRNAs (miR-429, miR-200b, and miR-200c) was increased more than 100-fold in 4T1 cells compared to 4TO7 cells. [score:2]
The 2 groups differ by a single seed nucleotide - miR-200b, miR-429 and miR-200c share the 5′-AAUACU-3′seed sequence and miR-200a and miR-141 have the 5′-AACACU-3′ seed. [score:1]
[1 to 20 of 8 sentences]
9
[+] score: 25
miR-204 and miR-488 (A) were down-regulated in Pkd1 [-/- ]kidneys whereas miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429 (B) were up-regulated in Pkd1 [-/- ]kidneys. [score:7]
Conversely, we found that up-regulation of miR-30a-5p, miR-96 and miR-182 at E17.5, and miR-429 at E14.5 were reciprocally correlated with down-regulation of Cpeb3, Sox6, Hdac9, and Ddx3y respectively in Pkd1 [-/- ]mutants (Additional file 21). [score:7]
Expression of 9 miRNAs (miR-204, miR-488, miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429), predicted to target significantly regulated genes at E14.5 was assayed using miRNA-qPCR. [score:5]
Expression of 9 miRNAs (miR-10a, miR-126-5p, miR-200a, miR-204, miR-429, miR-488, miR-96, miR-182 and miR-30a-5p), predicted to target significantly regulated genes at E17.5 was evaluated using miRNA-qPCR assays. [score:3]
We tested this hypothesis by determining the differential expression of 9 miRNAs (mmu-miR-10a, mmu-miR-30a-5p, mmu-miR-96, mmu-miR-126-5p, mmu-miR-182, mmu-miR-200a, mmu-miR-204, mmu-miR-429, and mmu-miR-488) between WT and Pkd1 [-/- ]genotypes at E14.5 and E17.5 (Figures 7 and 8). [score:3]
[1 to 20 of 5 sentences]
10
[+] score: 22
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-191, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-let-7d, 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-96, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, mmu-mir-449a, dre-mir-429a, 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-96, 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-140, dre-mir-141, dre-mir-152, 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, dre-let-7j, mmu-mir-449c, mmu-mir-449b, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-124b
As predicted from sequence analyses and thermal stability calculations, miR-141 MO specifically inhibited miR-200a and miR-141, miR-200b MO specifically inhibited miR-200b and miR-200c, and miR-429 MO specifically inhibited miR-429 (Figure S4B). [score:5]
Finally, 8 of 24 miRNA probes, including miR-200a and miR-200b, as well as miR-96, miR-141, miR-182, miR-183, miR-191, and miR-429, revealed robust expression in the MOE and VNO neuroepithelium, with weaker expression in the adjacent respiratory epithelium (Figure 2A, right column, and Table S3). [score:5]
Embryos injected with either miR-141/miR-200a or miR-200b/miR-429 pairs of antisense morpholinos showed lack of expression of the corresponding miR-200 members with a given 5′ seed but did not display any change in OMP expression relative to wild-type controls (data not shown). [score:5]
In addition, in situ hybridization analyses (Figure 7C) show that a mixture of all three morpholinos (Triple MO mix: miR-141 MO, miR-200b MO, and miR-429 MO) was sufficient to simultaneously inhibit the expression of all five mature zebrafish miR-200 family members to threshold levels of detection. [score:5]
One of these families, miR-200 family comprising miR-200a, miR-200b, miR-200c, miR-429, and miR-141, also highly detected by microarray, was among the most frequently cloned species in all olfactory tissues examined (Table S2). [score:1]
In order to test the specificity of each morpholino (MO) sequence, we systematically injected one-cell zebrafish embryos with either miR-141 MO, miR-200b MO, or miR-429 MO and performed in situ hybridization against all five miRNAs of the miR-200 family. [score:1]
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[+] score: 20
The top 15 differentially expressed microRNAs based on fold change (p<0.05) are presented in Table 1. The most differentially expressed miRNA was mmu-miR-429, a member of the miR-200 family, and 4 of the 5 miR-200f members (miR-141, miR-200b, miR-200c and miR-429) were in the top 15 differentially expressed miRNAs (shaded in Table 1). [score:7]
Quantitative RT-PCR was used to validate the differential expression of the miR-200 family and as shown in Table 2, all 5 members of the miR-200f (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) were expressed at significantly higher levels in the PMT samples compared to the RST samples. [score:4]
This family of microRNAs is expressed as two clusters on distinct chromosomes with the miR-200c/miR-141 cluster located on chromosome 12 in humans and chromosome 6 in mice and the miR-200b/miR-200a/miR-429 cluster located on chromosome 1 in humans and chromosome 4 in mice [15]. [score:3]
Expression (mean ± SEM) of miR-200a, miR-200b, miR-200c, miR-141 and miR-429 in RJ345 cells, RJ423 cells containing the empty vector control (RJ423EV) or RJ423 cells containing miR-200c (RJ423200c) as determined by Taqman RT-PCR. [score:3]
The seed sequence, the region of the miRNA that determines mRNA binding, is the same in miR-200b, miR-200c, and miR-429 (AAUACUG). [score:1]
One family of microRNAs that has garnered considerable attention in cancer biology is the miRNA-200 family (miR-200f) which consists of 5 members, miR-141, miR-200a, miR-200b, miR-200c and miR-429. [score:1]
miR-200a and miR-141 share the same seed sequence (AACACUG) that is different from the seed sequence of miR-200b, miR-200c and miR-429 by one nucleotide [16]. [score:1]
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[+] score: 18
Note increased proliferation (EdU) in the lingual (L) side to the tooth germ (in b, c, e), and the progression of epithelial morphogenesis (from cap to bell stage) after targeting miR-429-3p (b), miR-325-3p (c), and miR-200c-3p (e), whereas epithelial proliferation and morphogenesis were inhibited with miR-590-5p antagomir transfection, compared to off-target antagomir (a). [score:6]
In contrast to the results obtained after off-target antagomir transfection, mandibular explants, transfected with antagomirs targeting miR-429-3p, miR-325-3p, miR-590-5p, or miR-200c-3p exhibited striking changes in molar germ morphogenesis (Fig. 4a–e). [score:5]
Of note, loss-of-function using antagomirs targeting other miRNAs previously defined as part of the odontogenic miRNA signature (miR-429-3p and miR-325-3p, Fig. 4b,c) also produced increased epithelial and mesenchymal proliferation, compared to an antagomir off-target control. [score:4]
Our TLDA analysis of miRNA expression (Fig. 2a) revealed enriched expression of miR-429-3p, miR-325-3p, and miR-590-5p in molar tooth germs and developing incisors compared to SMGs, lungs and kidneys, which we confirmed using individual primers to detect the corresponding miRNAs (Fig. 2b–d; Suppl. [score:3]
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[+] score: 15
Five of these miRNAs were upregulated (miR-429, miR-200a, miR-200b, miR-200c and miR-10b) and one of them was downregulated (miR29-b) in the aggressive S2B11 clone compared to S2D10 (Figure 6A). [score:6]
We found that five miRNAs were significantly upregulated (miR-429, miR-200a, miR-200b, miR-200c and miR-10b) and one of them was significantly downregulated (miR-29b) in aggressive clone compared to non-aggressive one. [score:6]
MiR-200b, miR-200c and miR-429 were shown to be upregulated in DCIS lesions compared to normal breast tissues [23]. [score:3]
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[+] score: 13
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-28, 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, 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
For example, in mouse [14], miR-10b is highly expressed in spinal cord; miR-124 is wi dely expressed in brain tissues; miR-200b, miR-128a, miR-128b, miR-429 are specifically expressed in olfactory bulb; miR-200a is highly expressed in olfactory bulb; miR-7b is highly expressed in hypothalamus. [score:11]
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]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
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[+] score: 13
These included miR-8 family overexpressed in FCx and comprising of miRNAs from two chromosomal clusters, miR-429, miR-200a, miR-200a*, miR-200b, and miR-200b* from chromosome 4, and miR-141 and miR-200c from chromosome 6. Also, a chromosome 6 cluster with miR-182, miR-96, and miR-183 and a chromosome 11 cluster with miR-212 and miR-312 were expressed on a higher level in FCx. [score:5]
For example, in the ceramide pathway (Figure 5), miR132 and miR-212 were predicted to regulate Ras, Pi3k, Pp2a, and Tnfr1, miR-200a to regulate Nsmaf, Pp2a, and Map2k4, and miR-200b, miR-200c, and miR-429 to regulate Ras, Pp2a, Map3k1, and Jun. [score:4]
The Chipster tool was used to visualize the miR-8 family members located on chromosome 4 (miR-429, miR-200a, miR-200a*, miR-200b and miR200b*). [score:1]
As an example, Figure 3 shows visualization of miR-8 family (miR-429, miR-200a, miR-200a*, miR-200b and miR200b*) located on chromosome 4. 10.1371/journal. [score:1]
As an example, Figure 3 shows visualization of miR-8 family (miR-429, miR-200a, miR-200a*, miR-200b and miR200b*) located on chromosome 4. 10.1371/journal. [score:1]
0021495.g003 Figure 3The Chipster tool was used to visualize the miR-8 family members located on chromosome 4 (miR-429, miR-200a, miR-200a*, miR-200b and miR200b*). [score:1]
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[+] score: 12
To generate the vector expressing gfp under the control of the human miR-200b/miR-200a/miR-429 regulatory sequence we subcloned gfp from pCX-GFP into the pGL3-1574/ + 120 vector obtained from addgene. [score:4]
For b-e the qPCR values shown in the histograms result from 2 (b, d) or 3 (c, e) qPCR experiments (4 wells per condition in each experiment) (f) Electroporation of an expression construct driving GFP with regulatory sequences of the human miR-429/miR-200a/miR-200b cluster leads to GFP-labeled cells in the OB. [score:4]
In mice, three members (miR-429, miR-200a, miR-200b) reside in one intergenic cluster on chromosome 4. These showed particularly high expression levels (Fig. 1c). [score:3]
Finally, we introduced the human sequence upstream of the miR-200b/miR-200a/miR-429 cluster 29 upstream of a GFP-cassette. [score:1]
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[+] score: 12
These are the same stages during B-cell differentiation when expression of both ZEBs plummets (possibly due, in part, to HIF-1α also activating synthesis of miR-429 [37], a down-regulator of ZEB levels [38, 39]), and expression of Blimp-1α and XBP-1 dramatically increases. [score:8]
Differential expression of the miR-200 family microRNAs in epithelial and B cells and regulation of Epstein-Barr virus reactivation by the miR-200 family member miR-429. [score:4]
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[+] score: 11
MicroRNAs associated with the basal breast cancer subtype, including four members of the miR-17~92 family, miR-25 and miR-150, showed a distinctly different pattern, being equally distributed among clusters 1 and 2. Of particular interest was cluster 4, which in contrast to the global decrease in miRNA expression during lactation and involution showed a specific increase in expression during these stages, paralleled by a decrease in the expression of predicted targets for one of the cluster members, miR-429 (Additional file 7). [score:9]
The cluster includes miR-200 family members miR-200a, miR-141 and miR-429. [score:1]
This cluster included the seed-identical miRNAs miR-141 and miR-200a, and miR-429, which is situated in the same genomic cluster as miR-200a. [score:1]
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[+] score: 10
MiR-200b belongs to the miR-200 family and together with other family members miR-200a and miR-429, it is clustered in an intergenic region on human chromosome 1. MiR-200b is expressed in the epithelium during palatogenesis in the mouse, including in the midline epithelial seam (MES), and its expression gradually decreases as fusion proceeds (Shin et al., 2012a, b). [score:5]
MiR-200b belongs to the miR-200 family and together with other family members miR-200a and miR-429, it is clustered in an intergenic region on human chromosome 1. MiR-200b is expressed in the epithelium during palatogenesis in the mouse, including in the midline epithelial seam (MES), and its expression gradually decreases as fusion proceeds (Shin et al., 2012a, b). [score:5]
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[+] score: 10
However, the inhibitor to miR-429 was not as effective at knocking down miR-200c expression compared with inhibitors 200a and 200b, due to flanking sequence divergence of miR-429 (and the inhibitor). [score:9]
The following oligos were also used: miR-200a rf, 5′-TCGAATGACCACATCGTTACCAGACAGTGTTACTCGAGCTGC-3′ and miR-200a rr, 5′-GGCCGCAGCTCGAGTAACACTGTCTGGTAACGATGTGGTCAT-3′ miR-200b rf, 5′-TCGAATGACCTCATCATTACCAGGCAGTATTACTCGAGCTGC-3′ and miR-200b rr, 5′-GGCCGCAGCTCGAGTAATACTGCCTGGTAATGATGAGGTCAT-3′ miR-200c rf, 5′-TCGAATGACCTCCATCATTACCCGGCAGTATTACTCGAGCTGC-3′ and miR-200c rr, 5′-GGCCGCAGCTCGAGTAATACTGCCGGGTAATGATGGAGGTCAT-3′ miR-141 rf, 5′-TCGAATGACCCCATCTTTACCAGACAGTGTTACTCGAGCTGC-3′ and miR-141 rr, 5′-GGCCGCAGCTCGAGTAACACTGTCTGGTAAAGATGGGGTCAT-3′ miR-429 rf, 5′-TCGAATGACCACGGCATTACCAGACAGTATTACTCGAGCTGC-3′ and miR-429 rr, 5′-GGCCGCAGCTCGAGTAATACTGTCTGGTAATGCCGTGGTCAT-3′. [score:1]
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[+] score: 10
Other miRNAs from this paper: mmu-mir-141, mmu-mir-146a, mmu-mir-200b, mmu-mir-200a, mmu-mir-200c
Similarly, HG stimulation for 24 h caused a significant decrease in the miR-200a, miR-141, miR-200b, miR-200c, and miR-429 expression levels to 27, 18, 39, 71, and 39%, respectively, of the levels in the unstimulated control. [score:3]
As shown in Figure 2B, real-time PCR analyses showed that HG stimulation for 12 h resulted in a significant decrease in miR-200a, miR-141, miR-200b, miR-200c, and miR-429 expression levels to 53, 38, 11, 42, and 33%, respectively, of the levels in the unstimulated control. [score:3]
Similarly, 24 h HG stimulation decreased miR-200a, miR-141, miR-200b, miR-200c, and miR-429 expression levels to 27, 18, 39, 71, and 39% of the control level, respectively N = 5. ** p < 0.01 and *** p < 0.001 compared with control. [score:2]
P160808-004 G12; miR-429: Cat No. [score:1]
The five known miR-200 members are located on two chromosomes (chromosome 12: miR-141 and miR-200c; chromosome 1, miR-200a, miR-200b, and miR-429) and are highly conserved in higher vertebrates (Gheldof et al., 2012). [score:1]
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[+] score: 9
In addition the miR-429, a member of the miRNA-200 family, was upregulated 2-fold showing a similar trend of induction. [score:4]
We also observed the upregulation of 7 miRNAs belonging to the related and often co-transcribed miRNA-200 family (miR-200a,b,c/miR-141/miR-429) and miRNA-182 cluster (miR-182/miR-183), henceforth collectively referred to as miR-200/182. [score:4]
Interestingly, 6 members of the related and often co-transcribed miRNA-200 family (miR-200a,b,c/miR-141/miR-429) and miRNA-182 cluster (miR-182/miR-183), henceforth referred to collectively as miR-200/182, were amongst the highest induced in HSV-1 infected brain. [score:1]
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[+] score: 9
c-Myb activity is tightly regulated at different levels, including downregulation by several miRNAs: miR-150 [8], miR-15a [9], miR-34a [10], miR-126 [11], miR-200b, miR-200c and miR-429 [12] binding to its 3′ UTR. [score:5]
We therefore searched in the literature if some of miRNAs that have already been described to downregulate c-Myb via interacting with 3′ UTR, (miR-150, miR-15a, miR-34a, miR-126, miR-200b, miR-200c and miR-429), were activated during muscle differentiation. [score:4]
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In MDA-MB-231 cells expressing the OVOLs, we used to assess expression of miR-200 family members (miR-200a, miR-200b, miR-200c, miR-141, miR-429, miR205, miR-203), relative to controls miR-U6 and miR16. [score:5]
However, the expression of both OVOL TFs resulted in the induction of miR-429, miR-208 and miR-200c. [score:3]
The double-transduced cells showed greater than 2-fold increases in miR-200a, miR-200c, and miR-429 (Figure 6E), while only modest changes were seen in the single-transduced cells. [score:1]
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25
[+] 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-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
With exception of miR-33a, miR223, miR-9, miR-24, and miR-429, whose expression level was low in activated B cells, such Prdm1 -targeting miRNAs were significantly upregulated by HDI. [score:8]
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26
[+] score: 8
Recently, it has been shown that mir-200a, mir-200b, and mir-429 are up-regulated in the hypothalamus of ob/ob and db/db mice (Crépin et al., 2014). [score:4]
In the context of CNS, it has been shown that mir-200a, mir-200b, and mir-429 are up-regulated in the hypothalamus of ob/ob and db/db mice (Crépin et al., 2014). [score:4]
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27
[+] score: 8
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-200a, mmu-mir-200c
We confirmed significant downregulation of miR-141, miR-200a, miR-200b, miR-200c and miR-429 in ALK-TKI-resistant cells as determined by qRT-PCR (Figure 2B). [score:4]
By targeting ZEB1 and ZEB2, several members of the miR-200 family (miR-141, miR-200a, miR-200b, miR-200c and miR-429) are considered the main suppressors of EMT. [score:4]
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28
[+] score: 8
Fig. 4 Expression levels of miR-429 from control and antenatal MLPD groups. [score:3]
MLPD - Mice Offspring from the maternal low protein diet group To examine, whether the reduction in ACE-2 protein levels in the female antenatal MLPD group is as a consequence of reduced translation, we examined miRNA miR-429, which has a complementary binding site on 3’ UTR of ACE-2. Of importance, as shown in Fig.   4 miR-429 levels were significantly increased in the female and decreased in maleantenatal MLPD lungs, compared to controls. [score:2]
Importantly, there was no increase in ACE2 proteins and associated miRNA-429 in lungs from the male MLPD group. [score:1]
Of 10 miRNA suggested by the bio-informatics software, we chose mmu-mir-429 miRNA for the present study, by the use of the Context Score of more than 90 [th] percentile, as described by Grimson et al. [27]. [score:1]
As shown in the summary Fig.   5 and previous studies, we speculate that antenatal maternal protein restriction leads to increased miR-429, which causes reduced production of ACE-2 protein. [score:1]
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29
[+] score: 8
Concomitant with the large induction of epithelial -associated genes and repression of mesenchymal regulators, MET -associated miRNAs miR-205-5p and the miR-200 family (miR-200a-3p, miR-200b-3p, miR-200c-3p, miR-141-3p and miR-429-3p) [23- 26] were markedly upregulated (at least four-fold) in the Thy1- to SSEA1+ transition (Figure 2; Additional file 3). [score:5]
miRNAs associated with the MET (miR-200a, b, c-3p, miR-141-3p, miR-429-3p, miR-205-5p) [23- 26] were not differentially expressed between the piPSC lines and the stem cell lines, with the exception of miR-200c-3p. [score:3]
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30
[+] score: 8
The highest dysregulated miRNAs identified in the cMyBP-C related HCM mo del were the miR-192 and miR-429 for the upregulated, and the miR-451 and miR-301a for the downregulated. [score:8]
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31
[+] score: 7
We observed the upregulation of eight miRNAs that make up a related miR-200 family (miR-200a, 200b, 200c, miR-141, miR-429) and a miR-183/96/182 cluster. [score:4]
We noted a commonality between all three groups (PR+BC, PR+BC/CRIZ, and PR+BC/TOP): miR 200 family (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), miR-183/96/182 cluster, miR-30d-5p, and miR-191-5p were up-regulated, as compared to intact controls. [score:3]
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32
[+] score: 7
We could confirm that miR-200, miR-182, miR-183, miR-141, miR-96, miR-122 and miR-429 were indeed down regulated, and miR-34 and miR-206 were upregulated during hibernation torpor (Fig. 2B). [score:5]
We also report that two miRNA families, miR-200 family (miR-200a/miR-200b/miR-200c/miR-141/miR-429) and miR-182 family (miR-182/miR-183/miR-96), which were consistently lower in the brain samples from torpor phase ground squirrels compared to active animals, are involved in expression of various ULM proteins and their global protein conjugation. [score:2]
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33
[+] score: 6
Among them, miR-200a/b/c, miR-141, and miR-429 in the miR-200 family were significantly upregulated in early age AD in mice. [score:4]
MiR-200 family can be divided into two groups according to the seed sequences (group I: miR-141 and miR-200a; group II: miR-200b, miR-200c, and miR-429). [score:1]
Name of miRs/siRNAs Sequence miR-200a 5′-UAACACUGUCUGGUAACGAUGU miR-200b 5′-UAAUACUGCCUGGUAAUGAUGA miR-200c 5′-UAAUACUGCCGGGUAAUGAUGGA miR-141 5′-UAACACUGUCUGGUAAAGAUGG miR-429 5′-UAAUACUGUCUGGUAAUGCCGU miR-NC 5′-UAACGUGUCACGUCUCCGACUA Anti-miR-200c 5′-UAACACUUGCCGGGUAAUGGUGUA Anti-miR-NC 5′-UCUUGCCGGGCCCGAUCCAACGA siCont 5′-UUCUCCGAACGUGUCACGU siPTEN 5′-AACCCACCACAGCUAGAACUU 2.3 kb PTEN 3′UTR was amplified by PCR from a human cDNA library. [score:1]
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34
[+] score: 6
0068990.g001 Figure 1 (A) The expression of miR-200a, miR-200b and miR-429 in ES cell diferentiation. [score:3]
To determine whether miR-200 family is responsive to ES cell differentiation, we analyzed miR-200 mumbers (miR-200a, miR-200b and miR-429) expression during ES cell spontaneous differentiation by quantitative real-time PCR. [score:3]
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35
[+] score: 6
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-192, mmu-mir-200a, mmu-mir-200c
Several reports have shown that members of the miR-200 family (miR-200a,b,c, miR-141 and miR-429) inhibit EMT through direct targeting of ZEB1 and ZEB2, which encode transcriptional repressors of E-cadherin in kidney tubular cells [1], breast cancer cells [2], and mammary epithelial cells [3]. [score:6]
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36
[+] score: 6
The highly conserved miR-200 family is composed of five members, miR-200a, miR-200b, miR-200c, miR-141 and miR-429, which are similar in sequence and are clustered and expressed as two separate polycistronic pri-miR transcripts: the miR-200b/a/429 cluster on chromosome 4 and the miR-200c/141 cluster on chromosome 6. The miR-200 family has been reported to be strongly expressed in lung, kidney and thymus tissues [13]. [score:5]
Light gray bars, miR-200b; dark gray bars, miR-200a; black bars, miR-429. [score:1]
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37
[+] score: 6
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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
207 −0.414 142 −9.58 TRUE rno-miR-429 MIMAT0001538 1 8mer −0.176 −0.408 145 −11.68 TRUE rno-miR-30a-5p MIMAT0000808 1 offset 6mer −0.043 −0.1 142 −13.82 TRUE Identity: the name of the mature miRNA in miRBase v20. [score:1]
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38
[+] score: 5
For example, it was found that forced expression of miR-200a in meningioma cells [39], or expression of miR-429 in SW260 colorectal carcinoma cells [40], reduced xenograft tumor growth when injected into the flanks of SCID or nude mice, respectively. [score:5]
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39
[+] score: 4
However, miR-215 [31], miR-375 [32], miR-141, and miR-200c [33], miR-200a [34], miR-429 [35], miR-625 [36], and miR-18a [37] have already been shown to be inversely correlated with the EMT, and they were found downregulated in this subtype. [score:4]
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40
[+] score: 4
Similarly, five miRNAs (ssc-miR-192, 4_16129, 13_5595, ssc-miR-215 and ssc-miR-429) were significantly downregulated (Table 3). [score:4]
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41
[+] score: 4
Interestingly, among these miRNAs, miR-155 [19] and miR-429 [23] were shown to directly target HIF-1α mRNA 3’UTR, and found to be involved in HIF-1α negative-feedback loop. [score:4]
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42
[+] score: 4
The miRNA-200 family (miRNA-200a, miRNA-200b, miRNA-200c, miRNA-141 and miRNA-429) can inhibit tumor invasion and metastasis by regulating the EMT [33]. [score:4]
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43
[+] score: 4
Other miRNAs from this paper: mmu-mir-140, mmu-mir-200b, mmu-mir-200c
However, while miR-429 inhibited the luciferase activity and Pin1 protein levels as the same as miR-140-5p, miR-140-5p decreased Pin1 protein levels slightly more obvious than miR-429 (Fig. 1d and f). [score:3]
MiRNA-140-5p, miRNA-200b, miRNA-200c, miRNA-429 and NC mimics were synthesized by Genepharma (Shanghai, China). [score:1]
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44
[+] score: 4
Among the miRNAs upregulated in rat PSCs, we also identified miR-205 and members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429), which promote mesenchymal to epithelial transition (MET) in mouse cells, a key step in fibroblast reprogramming [47]. [score:4]
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45
[+] score: 4
Furthermore, recent reports suggest that the downregulation of several miRNAs (miR-200a, miR-200b, miR-200c, miR-141, and miR-429) is an essential feature of EMT [37]. [score:4]
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46
[+] score: 3
Our findings were in agreement with a recent report that the overexpression of miR-429, a member of the miR-200 family of microRNAs, in the mesenchymal-like ovarian cancer cells resulted in the mesenchymal–epithelial transition [33]. [score:3]
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47
[+] score: 3
In addition, previous studies have reported that miR-200b and miR-429 repress TGF-β1 -induced fibronectin expression in kidney proximal tubular and human primary mesothelial cells [51, 52]. [score:3]
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48
[+] score: 3
Other miRNAs from this paper: mmu-mir-200b, mmu-mir-205, mmu-mir-200a, mmu-mir-200c
However, Etv5 KD in OSKM combination only led to the decreased expression levels of miR-200a, miR-200b, and miR-429 (Fig.   3b). [score:3]
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49
[+] score: 3
Likewise, miR-200b and miR-429 predictably target BChE and AChE-R, and changes in their levels were reported under neuropathic pain following sciatic nerve ligation within the limbic forebrain's nucleus accumbens (Imai et al., 2011). [score:3]
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50
[+] score: 3
Elevated expression of miR-182 [39], miR-429 [40], miR-199a, 199a*, 200a, and 200b was positively and significantly correlated to the progression of liver fibrosis [41]. [score:3]
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51
[+] score: 3
In accordance, we found that expression of miR200a, miR200b, miR200c, miR429 and miR205 was significantly reduced in Pten [Δf]:p53 [Δf] versus Pten [Δf] tumors (Supplementary Fig S3B and C, Supplementary Table S1F). [score:3]
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52
[+] score: 3
The miR-200 family consists of five members (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), which are clustered and expressed as the miR-200b-200a-429 cluster at chromosomal location 1p36 and the miR-200c-141 cluster at chromosomal location 12p13. [score:3]
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53
[+] score: 3
The miRNA 200 family members, consisting of miR-200b, miR-200c, miR-429, miR-200a and miR-141, were considered to be tumor suppressor miRNAs in cancer development and progression [25, 26]. [score:3]
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54
[+] score: 3
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-200a, mmu-mir-34a, mmu-mir-200c
The miR-200 family, including miR-200a, miR-200b, miR-200c, miR-141 and miR-429, has been reported to be dysregulated in several types of cancers including gastric cancer, breast cancer and bladder cancer [20– 22]. [score:2]
As shown in Figure 1D, the levels of miR-200b and miR-200c, but not the levels of other members of the miR-200 family including miR-200a, miR-141 and miR-429, were obviously reduced in the livers of HFD-fed mice. [score:1]
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55
[+] score: 2
Consistent with our in vitro results, shDICER tumors expressed lower level of let-7b, miR-99b, miR-103a, and miR-200 miRNA family members (miR-429, miR-200c, miR-141 and miR-200b) compared to shControl tumors. [score:2]
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56
[+] score: 2
[29] miR-200b and miR-429 knockout mice have lower serum LH concentrations, an impaired LH surge, and failure to ovulate. [score:2]
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57
[+] score: 2
miR-429 regulates alveolar macrophage inflammatory cytokine production and is involved in LPS -induced acute lung injury. [score:2]
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58
[+] score: 2
In embryonic stem cells, c-Myc regulates miR-141, miR-200a and miR-429 to attenuate stem cell differentiation (Lin et al, 2009). [score:2]
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59
[+] score: 1
The miR-200 family contains miR-200a, miR-200b, miR-200c, miR-429, and miR-141 (Howe et al., 2012). [score:1]
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60
[+] score: 1
Hasuwa H., Ueda J., Ikawa M., Okabe M. (2013) miR-200b and miR-429 function in mouse ovulation and are essential for female fertility. [score:1]
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61
[+] score: 1
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-200a, mmu-mir-200c
The miR-200 family has five members: miR-200a, miR-200b, miR-200c, miR-141 and miR-429. [score:1]
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62
[+] score: 1
Nine sequences matched with mature miRNAs, 3 of them perfectly with mouse let-7b (MG030), let-7c (MG070) and human miR-923 (MG041) respectively, 3 with a 1-nt difference with mouse miR-126-5p (MG034), miR-429 (MG018) and human miR-1268 (MG068), and 3 have partial homologies (Additional file 1). [score:1]
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63
[+] score: 1
We selected the top 9 miRNAs (miR-200a, miR-200b, miR-182, miR-429, miR-183, miR-200c, miR-141, miR-96 and miR-24) showing the highest standard deviations. [score:1]
[1 to 20 of 1 sentences]
64
[+] score: 1
This miRNA family consists of five members (miR-200c, miR-141, miR-200a, miR-200b, and miR-429). [score:1]
[1 to 20 of 1 sentences]
65
[+] score: 1
Other miRNAs from this paper: mmu-mir-141, mmu-mir-200b, mmu-mir-200a, mmu-mir-200c
There were, however, no significant differences in the amounts of miR-200b, miR-200a, or miR-429 in MCF7 cells, cell culture medium, or exosomes (Additional file 1: Figure S8A–C). [score:1]
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66
[+] score: 1
The miRNAs in the pro-apoptotic category include miR-29a/b/c, miR-34a/b/c, let-7a/b/c/e/f/g/i, miR-141, miR-146, miR-203, miR-429, and several others. [score:1]
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67
[+] score: 1
Interestingly, miR-184, being the most highly enriched miRNA in the mature ducts was clustered tightly to a subset of epithelial specific miRNAs, which included members of the miR-183 family (miR-183, miR-96) and all members of the miR-200 family (miR-141, miR-200a, miR-200b, miR-200c and miR-429). [score:1]
[1 to 20 of 1 sentences]
68
[+] score: 1
Other miRNAs from this paper: hsa-mir-429
The Image:6309403 transcript (Figure 20Q, R) is predicted to encode microRNA 429 (mir429, GeneID: 723865) of unknown function [63]. [score:1]
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69
[+] score: 1
We have noticed that miRNAs are from mir-200 family (mir-200a, mir-200b and mir-429), mir-29 family (mir-29a and mir-29c) and mir-150 family, they are all related to lung cancer[60, 61]. [score:1]
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70
[+] score: 1
Other miRNAs from this paper: mmu-mir-135b
microRNA-429 -mediated silence of PP2A catalytic subunit, another AMPK phosphatase, also induced AMPK activation and protected cells from oxidative stress [29]. [score:1]
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71
[+] score: 1
MiR-141 is a member of the miR-200 family, which also includes miR-200a, miR-200b, miR-200c, miR-141, and miR-429. [score:1]
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72
[+] score: 1
In SM, miR-200b, miR-200a, and miR-429 were induced after LIF withdrawal (DM), an effect enhanced in NO (Supplementary Fig.   1c, middle upper graph) [28]. [score:1]
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73
[+] score: 1
MiR-200b and miR-429 function in mouse ovulation and are essential for female fertility. [score:1]
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74
[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
On contrary, four of liver-specific miRNAs reported here were reported in Kim et al. [9] as muscle (eca-miR-299, eca-miR-32, eca-miR-656) or colon-specific miRNAs (eca-miR-429). [score:1]
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The miR-200 family consists of 5 members localized on 2 genomic clusters, miR-200a/b, miR-429 and miR-200c, miR-141 on chromosomes 1 and 12 in humans and on chromosomes 4 and 6 in mice [22]. [score:1]
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Class TFS group Motif name miRNA name I 9.1001 MEF2A - 9.2002 FOXO, LEF1, STAT5B, POU1F1, NFAT, TLX-2, GATA-1, STAT5a, MAZ, IRF-7, TAF, FOXF2, JUN, FOXA1, FOXJ1, ZHX2 MIR-23B, MIR-144, MIR-142 6.0110 MEF2A - 15.2112 TGIF - IIa 8.0002 E2F, TCF3, ETS-2, PAX4 - IIb 4.0010 MEF2A - 4.0020 HOXA4, GCM1, RFX1, GATA3 MIR-24 13.2022 TAF - IIc 12.0022 TCF8, FOXO, TAF MIR-524 IIIa 1.1000 STAT5B, STAT5A, PGR, LEF1, TCF3, FOXF2, E4F1 MIR-124A, MIR-17-5P, MIR-20A, MIR-106A, MIR-106B, MIR-20B, MIR-519D", MIR-182, MIR-200B, MIR-200C, MIR-429, MIR-202, MIR-199A, MIR-519E, MIR-9 IIIb 2.0100 MYCN, OLF1, MYOD1 - 2.0200 - MIR-493 - 11.1101 LEF1 -Motifs and miRNAs within each TFS group are listed in order of decreasing enrichment p-value, based on data provided in Additional file 3, Table S3B. [score:1]
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MiR-200b and miR-429 function in mouse ovulation and are essential for female fertility. [score:1]
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41 mmu-miR-33 −59.71 mmu-miR-222 1.23 mmu-miR-93 −1.52 mmu-miR-124 −97.01 mmu-miR-429 1.07 mmu-miR-192 −1.52 mmu-miR-129-5p −111.43 mmu-miR-100 −1.74 mmu-miR-210 −157.59 mmu-miR-20a −2 mmu-miR-134 −194.01 mmu-miR-137 −2 mmu-miR-215 −222.86 mmu-miR-194 −2.14 mmu-miR-452 −675.59 mmu-miR-196a −2.64 mmu-miR-223 −955.43 Differentiated sample versus control sample [DIF EBs d8/CONTROL EBs d8]. [score:1]
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In this study, many miRNAs associated with azoospermia, such as miR-199a-5p 21, miR-181a 22, miR-221 23, miR-141 19, and miR-429 19 24, were found to be significantly modulated by exposure to MC-LR (Table 1). [score:1]
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One cluster resides on human chromosome 1 and encodes miR-200b, miR-200a, and miR-429, while the other cluster is located on human chromosome 12, and encodes miR-200c and miR-141. [score:1]
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