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10 publications mentioning dre-mir-145

Open access articles that are associated with the species Danio rerio and mention the gene name mir-145. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 576
Interestingly, miR-145 expression is downregulated in liver cancer, and restoration of miR-145 expression in liver tumor cells results in inhibition of proliferation in these cells [21, 22]. [score:10]
The quantification of mRNA expression levels using qPCR revealed that hhex expression at 30 hpf and sePb expression at 50 hpf did not exhibit significant changes under miR-145 mimic and inhibitor administration. [score:9]
At 72 hpf, WISH indicates normal miR-145 expression in control -injected fish (A and B), reduced miR-145 expression in miR-145 inhibitor -injected fish (C and D) and overexpression of miR-145 in miR-145 mimic -injected fish (E and F). [score:9]
miR-145 inhibitor -injected embryos had increased prox1 expression and miR-145 mimic -injected embryos had reduced prox1 expression at 72 hpf (Fig 4G–4I). [score:7]
In contrast, at hepatic outgrowth stages, loss of miR-145 increases prox1 and fabp10 expression, while overexpression of miR-145 decreases prox1 and fabp10 expression. [score:7]
S4 FigLiver morphology was determined by EGFP expression in Tg(fabp10: EGFP) embryos at 4 dpf (A) or in embryos injected with control mimic (B); miR-145 inhibitor (C); miR-145 mimic (D); miR-145 inhibitor with three doses of grnA MO 0.0625 ng/embryo (E), 0.125 ng/embryo (F), or 0.25 ng/embryo (G); and miR-145 mimic with three doses of grnA mRNA 0.1 ng/embryo (H), 0.2 ng/embryo (I), or 0.4 ng/embryo (J). [score:7]
After 3ng miR-145 inhibitor injection, miR-145 inhibition significantly increased the size of liver expressing EGFP at 4 dpf (Fig 3B). [score:7]
To test the specificity, we determined the expression level of Gata6, which is a known target of miR-145 [28], in miR-145 mimic- and inhibitor -injected fish. [score:7]
0177887.g008 Fig 8Liver morphology was determined by EGFP expression at 4 dpf in Tg (fabp10: EGFP) embryos (A) or in embryos injected with control mimic (B), miR-145 inhibitor (C), miR-145 mimic (D), miR-145 inhibitor with grnA MO (0.25 ng/embryo) (E) and miR-145 mimic with grnA mRNA (0.4 ng/embryo) (F). [score:7]
To study the regulatory mechanism of miR-145 in embryonic liver development, we blocked the mature miR-145 function using a miR-145 hairpin inhibitor and enhanced miR-145 expression using a miR-145 RNA mimic. [score:7]
Liver morphology was determined by EGFP expression at 4 dpf in Tg (fabp10: EGFP) embryos (A) or in embryos injected with control mimic (B), miR-145 inhibitor (C), miR-145 mimic (D), miR-145 inhibitor with grnA MO (0.25 ng/embryo) (E) and miR-145 mimic with grnA mRNA (0.4 ng/embryo) (F). [score:7]
Furthermore, fabp10 expression also increased in miR-145 inhibitor -injected embryos at 96 hpf, while, inversely, fabp10 expression decreased in miR-145 mimic -injected embryos at 96 hpf (Fig 4J–4L). [score:7]
miR-145 and GrnA expression patterns are inversely correlated during liver developmentFluorescence in situ hybridization (FISH) was used to determine the miR-145 and GrnA expression patterns specifically in liver development. [score:7]
We reason that loss or attenuation of miR-145 expression promotes hepatic proliferation and liver outgrowth, and inversely, miR-145 overexpression suppresses hepatic proliferation and liver growth. [score:7]
The proxl expression at 72 hpf and fabp10 expression at 96 hpf increased by 1.5-fold and 2.9-fold, respectively, in miR-145 inhibitor -injected embryos. [score:7]
In addition, we find an inverse correlation between miR-145 downregulation and GrnA overexpression in zebrafish liver outgrowth. [score:6]
miR-145 is a tumor suppresser miRNA that is significantly downregulated in many cancers and contributes to tumor cell growth [19– 22]. [score:6]
At 24 hours after control mimic, miR-145 inhibitor and miR-145 mimic (100 nM) treatments in ZFL cells, the mRNA expression levels of GrnA and MET increased in ZFL cells treated with miR-145 inhibitor as compared to those in control -treated cells. [score:6]
In contrast, GrnA and MET were downregulated in miR-145 -overexpressing ZFL cells (Fig 7A). [score:6]
In addition, the qPCR analysis reveals that gata6 expression is regulated by altered expression of miR-145 (H). [score:6]
Our findings reveal that the mRNA and protein expression levels of GrnA are inversely regulated in response to the loss and overexpression of miR-145. [score:6]
miR-145 is downregulated and serves as a tumor suppressor microRNA in many types of cancers, such as breast [47], ovary [48], liver [19] and colon cancers [49]. [score:6]
miR-145 mimic and miR-145 hairpin inhibitor treatment specificity and efficiently regulate miR-145 expression in vivo. [score:6]
miR-145 directly targets and modulates GrnA expression. [score:6]
miR-145 downregulation and PGRN overexpression are required for liver tumor cell proliferation. [score:6]
The percentage of PCNA -positive hepatocytes was increased by 2.4-fold in response to miR-145 inhibition in embryos at 4 dpf: 36.7 ± 6.7% in the control versus 90 ± 10% in the miR-145 inhibitor -injected fish (Fig 5E and 5G). [score:5]
miR-145 expression in the liver primordium decreases from 30 to 96 hpf and GrnA expression increases from 30 to 96 hpf. [score:5]
S1 FigThe miR-145 expression pattern at 72 hpf was examined using WISH and qPCR in control-, miR-145 inhibitor- and miR-145 mimic -injected fish. [score:5]
The expression level of Gata6 showed a 2.4-fold increase in miR-145 inhibitor -injected fish and a 0.6-fold decrease in miR-145 mimic -injected fish (S1H Fig). [score:5]
The miR-145 inhibitor- and miR-145 mimic -injected embryos exhibited a normal expression pattern of hhex at 30 hpf (Fig 4A–4C). [score:5]
These results suggest that the mimic and inhibitor treatments specificity and efficiently modulate miR-145 expression. [score:5]
However, the expression of hhex, a marker for liver specification, is affected neither by the loss of miR-145 nor by miR-145 overexpression. [score:5]
The expression levels of the grnA and met genes were examined using qPCR after 24 hours of control, miR-145 mimic and miR-145 inhibitor treatment in ZFL cells (A). [score:5]
The qPCR analysis reveals that the miR-145 mimic and inhibitor modulate miR-145 expression (G). [score:5]
Luciferase activity was suppressed approximately 45% when miR-145 was co-expressed with the psi-grna vector, but there was no significant effect on the mutant control (Fig 6B). [score:5]
In addition, quantitative real-time PCR (qPCR) of miR-145 showed that apparent miR-145 was significantly decreased after miR-145 inhibitor injection and that apparent miR-145 expression was increased approximately thirty fold after miR-145 mimic injection (S1G Fig). [score:5]
After miR-145 inhibitor and mimic injection, the dose -dependent alteration of the size of liver expressing EGFP at 4 dpf was observed. [score:5]
In tumor growth, restoration of miR-145 inhibits the PI3K/Akt pathway and suppresses cell growth [50]. [score:5]
The miR-145 expression pattern at 72 hpf was examined using WISH and qPCR in control-, miR-145 inhibitor- and miR-145 mimic -injected fish. [score:5]
0177887.g007 Fig 7The expression levels of the grnA and met genes were examined using qPCR after 24 hours of control, miR-145 mimic and miR-145 inhibitor treatment in ZFL cells (A). [score:5]
In this study, we decide to determine whether the direct target gene of the miRNA is useful for studying the biological function of miR-145 during liver development. [score:5]
The result reveals mesoderm development was not significantly affected by manipulation of miR-145 expression (A). [score:4]
miR-145 regulates GrnA and MET gene expression. [score:4]
Expression of certain specific markers at different liver developmental stages is affected by miR-145. [score:4]
The differentiation marker selenoprotein Pb (sePb) was detected at 50 hpf and also exhibited a normal expression pattern in miR-145 inhibitor- and miR-145 mimic -injected embryos as compared to those in controls (Fig 4D–4F). [score:4]
We hypothesize that hepatocyte outgrowth is the major target of miR-145 during liver development and that the process of hepatic proliferation is activated in the outgrowth stages. [score:4]
Following miR-145 inhibition, the results showed that GrnA and MET protein expression levels increased by 1.2-fold and 1.5-fold, respectively, as compared to those in control mimic treatment in ZFL cells. [score:4]
In situ hybridization using an LNA antisense probe against mature miR-145 indicated that the miR-145 inhibitor reduced the level of miR-145 (S1C and S1D Fig) and miR-145 mimic treatment increased miR-145 expression (S1E and S1F Fig) compared to that seen in control mimic -injected fish at 72 hpf (S1A and S1B Fig). [score:4]
In contrast, embryos with overexpression of miR-145 exhibited smaller EGFP -expressing liver compared to that seen in control -injected liver (Fig 3A and 3C). [score:4]
The EGFP expression of Tg (fabp10: EGFP) fish showed an enlarged liver in miR-145 inhibitor -injected fish and an underdeveloped liver in miR-145 mimic -injected fish fish as compared to that in control fish. [score:4]
In this process, miR-145 directly targets the mRNA of GrnA, and GrnA rescues the miR-145 -induced liver defect. [score:4]
miR-145 and GrnA expression patterns are inversely correlated during liver development. [score:4]
Taken together, we identify a new role of miR-145 that is required for hepatic outgrowth through regulating GrnA expression. [score:4]
In contrast, GrnA and MET protein expression levels reduced by 0.7-fold and 0.4-fold, respectively, in miR-145 -overexpressing ZFL cells as compared with those in control mimic -treated cells (Fig 7B). [score:4]
miR-145 expression level negatively regulates embryonic liver size. [score:4]
MiR-145 inhibits cell proliferation of human lung adenocarcinoma by targeting EGFR and NUDT1. [score:4]
Fluorescence in situ hybridization (FISH) was used to determine the miR-145 and GrnA expression patterns specifically in liver development. [score:4]
In conclusion, these whole-mount and qPCR data indicate that miR-145 expression has major effects on hepatic outgrowth stage during liver development. [score:4]
To determine whether GrnA is a direct target of miR-145 in mediating hepatic outgrowth, we conducted bioinformatics software prediction using MicroInspector[26] and RNAhybrid [27] to identify the putative miR-145 recognition site located in exon 20 of the GrnA. [score:4]
miR-145 and GrnA expression patterns are inversely correlated during liver development. [score:4]
To study the influence of miR-145 in liver development, the 1.5 ng and 3 ng of control, miR-145 mimic or miR-145 inhibitor was injected into Tg(fabp10: EGFP) zebrafish. [score:4]
The developmental growth is normal under altered expression of miR-145. [score:4]
These results indicate that miR-145 and GrnA expression are inversely correlated during liver development. [score:4]
The miR-145 inhibitor is 2′-O-methyl antisense oligonucleotides that against miR-145 were synthesized by Dharmacon RNA Technologies. [score:3]
The 3 ng/embryo of control mimic (5’-UCACAACCUCCUAGAAAGAGUAGA-3’), 1.5 and 3 ng/embryo miR-145 mimic (5’-GUCCAGUUUUCCCAGGAAUCCCU-3’), 3 ng/embryo miR-9 mimic (5’-UCUUUGGUUAUCUAGCUGUAUGA-3’), 0.03ng/embryo miR-206 mimic (5′-UGGAAUGUAAGGAAGUGUGUGG-3’), 3 ng/embryo miR-731 mimic (5’-AAUGACACGUUUUCUCCCGGAUCG-3’), 3 ng/embryo miR-217 mimic (5’-UACUGCAUCAGGAACUGAUUGG-3’) and 1.5 and 3 ng/embryo miR-145 inhibitor (Dharmacon, Thermo) were injected into one-cell stage embryos. [score:3]
The EGFP expression of Tg (fabp10: EGFP) fish showed no significantly changes in liver size in miR-9 mimic-, miR-206 mimic-, miR-731 mimic- and miR-217 mimic -injected fish, but the miR-145 mimic -injected fish has a smaller liver size (Fig 1B). [score:3]
miR-145 directly targets grnA as determined by luciferase assay. [score:3]
Similar gene expression patterns of miR-145 and PGRN also occur in pathological liver growth. [score:3]
Co-injection of the miR-145 inhibitor with 0.25 ng/embryo GrnA morpholino in Tg(fabp10: EGFP) embryos restored normal liver size (Fig 8E). [score:3]
In this study, we show that miR-145 targets GrnA in attenuating zebrafish liver outgrowth. [score:3]
The expression levels of miR-145, GrnA and MET signaling were measured in zebrafish embryos treated with control, miR-145 mimic or miR-145 hairpin inhibitor using a High Capacity cDNA Reverse Transcription kit and Power SYBR Green PCR master Mix (Applied Biosystems). [score:3]
We demonstrate that miR-145, which targets the CDS region of GrnA, can affect embryonic liver growth. [score:3]
miR-145 was expressed in hepatoblasts at 30 and 50 hpf but decreased at 72 and 96 hpf (Fig 2A). [score:3]
Furthermore, in humans, PGRN is also a predicted target of miR-145. [score:3]
The luciferase activity of psi-grna-WT was suppressed approximately 45% in response to miR-145 mimic treatment. [score:3]
To control for the specificity of the miR-145 mimic and inhibitor, a negative control mimic was used, the sequence of which was based on C. elegans microRNAs that have minimal sequence identity to zebrafish. [score:3]
Smaller liver sizes were observed at 96 hpf in miR-145 overexpressing- Tg(fabp10: EGFP) fish (Fig 8D). [score:3]
We also demonstrate an inverse correlation between miR-145 and GrnA expression during hepatogenesis. [score:3]
Inversely, fabp10 expression at 96 hpf showed a 0.5-fold decrease in miR-145 mimic -injected embryos (Fig 4M). [score:3]
0177887.g003 Fig 3Liver morphology at 4 dpf after control mimic (A), miR-145 inhibitor (B) and miR-145 mimic (C) injections in Tg(fabp10:EGFP) embryos. [score:3]
The protein levels of GrnA, MET and GAPDH were examined by Western blotting in ZFL cells at 48 hours after control, miR-145 mimic and miR-145 inhibitor treatments. [score:3]
The liver sections of control mimic-, miR-145 inhibitor- and miR-145 mimic -injected fish were examined using PCNA staining at 4 dpf. [score:3]
These data suggest that miR-145 modulates GrnA expression through binding to GrnA mRNA in zebrafish liver. [score:3]
In the rescue experiments, we show that GrnA expression rescues the hepatic outgrowth defect caused by miR-145 manipulation. [score:3]
0177887.g004 Fig 4A WISH assay was used for determination of the liver developmental markers hhex at 30 hpf (A-C, dorsal view), sePb at 50 hpf (D-F, dorsal views), prox1 at 72 hpf (G-I, dorsal views) and fabp10 at 96 hpf (J-L, dorsal views) in control, miR-145 inhibitor -injected and miR-145 mimic -injected embryos. [score:3]
ZFL cells were transfected in six-well plates with miR-145 mimic (final concentration 100 nM), miR-145 hairpin inhibitor (final concentration 100 nM) or miR-control (final concentration 100 nM). [score:3]
0177887.g002 Fig 2(A,B) The expression patterns of miR-145 (A), grnA (B) and the hepatoblast-specific marker gene prox1 at 30, 50, 72 and 96 hpf were examined using FISH in wild-type zebrafish embryos. [score:3]
Furthermore, we determine whether endogenous GrnA expression is affected by miR-145. [score:3]
miR-145 is ubiquitously expressed at 19-somite zebrafish embryos as demonstrated by Zeng et al. [28]. [score:3]
These results indicate that miR-145 expression level negatively affects liver size at 4 dpf in zebrafish. [score:3]
The liver size of miR-145 inhibitor -injected Tg(fabp10: EGFP) embryos increased by approximately 170% (3.4 ± 0.6×10 [-3]mm [3]); however, the liver size of miR-145 mimic -injected Tg(fabp10: EGFP) embryos reduced to 25% of the liver size of the control group (0.5± 0.1×10 [-3]mm [3]) (Fig 3G). [score:3]
Taken together, our findings indicate that miR-145 regulates GrnA -dependent hepatic outgrowth in zebrafish development. [score:3]
A total of 3 ng of control, miR-145 inhibitor or miR-145 mimic was injected into wild-type zebrafish embryos. [score:3]
0177887.g005 Fig 5 The liver sections of control mimic-, miR-145 inhibitor- and miR-145 mimic -injected fish were examined using PCNA staining at 4 dpf. [score:3]
To analyze the liver specific expression pattern of miR-145 and GrnA, we isolated the fetal liver at 72 and 96 hpf to perform qPCR. [score:3]
The liver morphology in 3 ng miR-145 mimic and inhibitor treatment was significantly affected (S2 Fig). [score:3]
Importantly, the results of the luciferase activity assay suggest that miR-145 directly targets GrnA. [score:3]
Numerous reports have indicated that miR-145 is a suppressor of tumor cell proliferation in various types of cancers [36– 39], including liver cancer [40]. [score:3]
miR-145 is expressed in liver of zebrafish embryos at 30 hpf. [score:3]
0177887.g006 Fig 6The predicted miR-145 target site on GrnA CDS is illustrated. [score:3]
Consequently, miR-145 expression attenuates cell proliferation in embryonic liver. [score:3]
The dose -dependent effects of miR-145 mimic and inhibitor on hepatic outgrowth. [score:3]
The predicted miR-145 target site on GrnA CDS is illustrated. [score:3]
A WISH assay was used for determination of the liver developmental markers hhex at 30 hpf (A-C, dorsal view), sePb at 50 hpf (D-F, dorsal views), prox1 at 72 hpf (G-I, dorsal views) and fabp10 at 96 hpf (J-L, dorsal views) in control, miR-145 inhibitor -injected and miR-145 mimic -injected embryos. [score:3]
S2 FigLiver morphology at 4 dpf after 1.5 ng and 3 ng control mimic, miR-145 inhibitor, miR-145 mimic injection in Tg(fabp10: EGFP) embryos. [score:3]
ZFL cells (~5×10 [5]) were co -transfected with miR-145 mimic (50 nM) or control mimic (50 nM) and target reporter plasmid (1.6 μg) using LipofectamineTM 2000 (Invitrogen). [score:3]
Liver morphology at 4 dpf after control mimic (A), miR-145 inhibitor (B) and miR-145 mimic (C) injections in Tg(fabp10:EGFP) embryos. [score:3]
Wienholds’s and Zeng’s groups have proved that miR-145 is expressed in gut but not in liver of zebrafish embryos at 96 hpf [28, 33]. [score:3]
The expression pattern of miR-145, especially in the embryonic liver, has not been confirmed. [score:3]
To determine whether miR-145 affects embryonic hepatic outgrowth through targeting GrnA, we performed GrnA mRNA and morpholino rescue experiments to verify whether GrnA signaling can rescue the miR-145 -induced liver defect. [score:3]
miR-145 mimic, miR-145 hairpin inhibitor and negative-control mimic were purchased from Dharmacon (Thermo). [score:3]
Control mimic, miR-145 inhibitor and miR-145 mimic were transfected into ZFL cells to assess the activation of GrnA and MET signaling using qPCR and Western blotting. [score:3]
This study is the first to show that the manipulation of miR-145 expression affects embryonic liver size. [score:3]
Furthermore, we show that miR-145 is almost not expressed in zebrafish embryos at 96 hpf. [score:3]
From microRNA prediction targeting GrnA using bioinformatics software, we have identified a microRNA, miR-145. [score:3]
Co-injection of miR-145 inhibitor with GrnA morpholino restored normal liver size (1.8 ± 0.2×10 [-3]mm [3]); similarly, co-injection of miR-145 mimic and GrnA mRNA also restored normal liver size (2.2 ± 0.2×10 [-3]mm [3]) (Fig 8G). [score:3]
We show that manipulation of miR-145 has minor effects on the expression of specification- and differentiation-related genes. [score:3]
For further study, we propose that miR-145 targeting of PGRN may contribute to tumor cell growth in cancer progression. [score:3]
These data suggest that miR-145 regulates cell proliferation and embryonic hepatic outgrowth. [score:2]
The EGFP expression of Tg (fabp10: EGFP) fish showed a smaller liver phenotype in miR-145 mimic -treated fish compared to wild type, control fish and other miRNAs mimic -treated fish. [score:2]
Taken together, these results suggest that miR-145 and PGRN regulate the same downstream signaling pathways-the MEK/Erk and PI3K/Akt pathways. [score:2]
miR-145 inhibitor -injected fish had more PCNA -positive hepatocytes (B, E) as compared to those in control (A,D). [score:2]
The quantification of liver volume showed enlarged liver (3.4± 0.6×10 [-3]mm [3]) in miR-145 inhibitor -injected fish and smaller liver (0.5± 0.1×10 [-3]mm [3]) in miR-145 mimic -injected fish as compared with normal livers in WT and control mimic -injected fish (2.0 ± 0.4×10 [-3]mm [3] and 2.0 ± 0.5×10 [-3]mm [3], respectively). [score:2]
These were co -injected with miR-145 mimic or inhibitor for the rescue assay. [score:2]
Although miR-145 has been shown to be involved in liver cancer progression, the functional roles of miR-145 in embryonic liver development are still unknown. [score:2]
In contrast, the PCNA -positive hepatocytes of embryos with miR-145 overexpression showed a 1.8-fold reduction compared to those in controls at 4 dpf: 36.7 ± 6.7% in the control versus 20 ± 3.3% cells in miR-145 mimic -injected fish (Fig 5F and 5G). [score:2]
It is possible that the miR-145 and PGRN regulatory mechanism is conserved. [score:2]
Whole-mount in situ hybridization (WISH) was used to clarify the stages of liver development affected by miR-145. [score:2]
miR-145 directs intestinal maturation in zebrafish. [score:2]
miR-145 is required for hepatic outgrowth during liver development. [score:2]
In the present study, we reveal that miR-145 regulates embryonic liver size by controlling hepatocyte proliferation. [score:2]
At the same time, MET gene is also inversely regulated by miR-145. [score:2]
Our results suggest that the relevant mechanisms of miR-145 -mediated growth regulation may exist in both embryonic hepatic growth and liver tumor growth. [score:2]
The regulatory mechanism of miR-145 and GrnA is important not only in physiological liver growth but also in pathological liver growth. [score:2]
The qPCR result reveals that the expression of miR-145 in embryonic liver at 96 hpf decreased as compared to that at 72 hpf. [score:2]
miR-145 is one of that affects embryonic liver growthTo identify the fine-tuning regulator of GrnA -mediated MET signaling, we identified several microRNAs (miRNAs) from the miRNA predictions of GrnA using bioinformatics software. [score:2]
Consequently, we show that miR-145 may serve as a novel regulator of GrnA to modulate hepatic outgrowth. [score:2]
miR-145 knockdown resulted in a significant increase in liver size at 96 hpf in Tg(fabp10: EGFP) fish (Fig 8C). [score:2]
These results suggest that miR-145 modulates embryonic liver outgrowth through regulating GrnA signaling. [score:2]
The regulatory mechanism between miR-145 and GrnA in hepatic outgrowth. [score:2]
We have found that the coding region of GrnA has a near perfect complementary binding site for the miR-145 seed region. [score:1]
Liver morphology at 4 dpf was observed after injecting control mimic, miR-145 mimic, miR-9 mimic, miR-206 mimic, miR-731 mimic and miR-217 mimic in Tg(fabp10: EGFP) embryos. [score:1]
The physiological role of miR-145 in hepatogenesis remains unknown. [score:1]
In contrast, a low signal was detected in response to miR-145 mimic treatment (C,F). [score:1]
First we made a construct containing the putative miR-145 recognition site behind a luciferase reporter (psi-grna vector, Fig 6A). [score:1]
Our results indicate an important role of miR-145 in modulating hepatic outgrowth. [score:1]
In contrast, the luciferase activity of psi-grna-mutant was unchanged in response to miR-145 mimic treatment (*P < 0.05, t-test) (B). [score:1]
miR-145 modulates hepatocyte proliferation in zebrafish embryos. [score:1]
miR-145 is one of miRNAs prediction on zebrafish GrnA that affects embryonic liver growth. [score:1]
GrnA rescues the hepatic outgrowth defect caused by miR-145 manipulation. [score:1]
The three doses of GrnA rescue the hepatic outgrowth defect caused by miR-145 manipulation. [score:1]
However, we cannot exclude the possibilities of miR-145 involvement in hepatic specification and/or differentiation. [score:1]
The miR-145 on GrnA CDS region was predicted by MicroInspector [26] and RNAhybrid [27]. [score:1]
These findings suggest that only miR-145 can affect embryonic liver growth among the predicted miRNAs of GrnA. [score:1]
GrnA can rescue the defect in liver outgrowth in miR-145 morphants. [score:1]
These data suggest that miR-145 binds the putative miR-145 recognition site of GrnA in transfected ZFL cells. [score:1]
0177887.g001 Fig 1 miR-145 is one of that affects embryonic liver growth. [score:1]
To investigate whether miR-145 is involved in embryonic hepatic outgrowth through controlling cell proliferation, we performed immunohistochemistry with an antibody against proliferating cell nuclear antigen (PCNA) to observe cell proliferation in liver sections at 4 dpf in control mimic-, miR-145 mimic- and miR-145 inhibitor -injected fish. [score:1]
miR-145 is critical for liver morphogenesis. [score:1]
A mutant control was generated with the luciferase reporter vector followed by four nucleotides mutant at the putative miR-145 recognition site region. [score:1]
The body length were measured at 96 hpf after control mimic, miR-145 inhibitor, miR-145 mimic injection in Tg(fabp10: EGFP) embryos (B). [score:1]
The miRNA predictions of GrnA included miR-9, miR-206, miR-731, miR-217 on 3’UTR and miR-145 on CDS region (Fig 1A). [score:1]
miR-145 influences hepatocyte proliferation in zebrafish embryos. [score:1]
Fluorescence-labeled RNA probes of the hepatoblast-specific marker prospero-related homeobox 1 (prox1) and DIG-labeled miR-145 or GrnA RNA probes were detected at 30, 50, 72 and 96 hpf in wild-type (AB) zebrafish embryos. [score:1]
miR-145 also reduces MEK/Erk signaling in tumor cells [51]. [score:1]
miR-145 is required for hepatic outgrowth. [score:1]
miR-145 5’ and 3’ DIG-labeled LNA probes (Exiqon) were used for miRNA in situ hybridization. [score:1]
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miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 MiRNAs are small, 19–23 nucleotide non-coding RNAs that function as post-transcriptional repressors of gene expression, either through messenger RNA (mRNA) degradation or translational repression (Bartel, 2009). [score:14]
miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 Using microarray analysis, the expression profile of murine miRNAs in the developing lip and PS were analyzed from E10 to E14 (Mukhopadhyay et al., 2010; Warner et al., 2014). [score:12]
miRNA gene or target mRNA Species Genome variation Molecular effect PDGFRa Human Mutation 3′UTR Altered miR-140 bindingRattanasopha et al., 2012 miR-140 Human SNP Altered miRNA-140 processingLi et al., 2010, 2011 Zebrafish Overexpression Altred Pdfra repressionEberhart et al., 2008 MSX1 Human SNP 3'UTR Altered miR-3649 bindingMa et al., 2014 FGF2/5/9 Human SNP3'UTR Altered miR-496/miR-145/miR-187 bindingLi D. et al., 2016 miR-17-92 cluster Mouse Homozygous deletion Altered Tbx113, Fgf10, Shox2 & Osr1 repressionWang et al., 2013 miR-200b Mouse Overexpression Altered Smad2, Snail& Zeb112 repressionShin et al., 2012a, b miR-133b Zebrafish Overexpression UnkownDing et al., 2016 CS, CC, JV: Conception of the work, drafting of the manuscipt, revision of the manuscript, final approval of the manuscript. [score:10]
Similarly, altered miR-496-FGF2, miR-145-FGF5, and miR-187-FGF9 interactions were associated with clefting in 289 nsCLP and 49 nsCPO patients (Li D. et al., 2016). [score:1]
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Interestingly, miR-145 also participates in a regulatory loop involving the tumor suppressor p53 and targets ER-alpha in human breast cancer cells [32], and the processing of the primary miRNAs (pri-miRNAs) of miR-143 and miR-145 by Drosha was also shown to be regulated in a p53 -dependent manner [33]. [score:7]
MiR-143 and miR-145 are co-expressed miRNAs that function as tumor suppressors and their repression by k-Ras potentiates the oncogenic k-Ras signaling by a feed-forward loop [30, 31]. [score:5]
Spizzo R. Nicoloso M. S. Lupini L. Lu Y. Fogarty J. Rossi S. Zagatti B. Fabbri M. Veronese A. Liu X. miR-145 participates with TP53 in a death-promoting regulatory loop and targets estrogen receptor-alpha in human breast cancer cellsCell Death Differ. [score:4]
Cui S. Y. Wang R. Chen L. B. MicroRNA-145: A potent tumour suppressor that regulates multiple cellular pathwaysJ. [score:3]
Noticeably, several of the estrogen-repressed miRNAs (miR-26, miR-107, miR-126 and miR-145) were also reduced by the physiological estrogen levels of vitellogenic females [8]. [score:1]
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[+] score: 6
Moreover, the direct miRNA targets of P53, that were dre-miR-34a, dre-miR-145 and dre-miR-15a [41], were differentially expressed in RPL5 MO zebrafish when compared with the Control. [score:5]
For example, miR-145 and miR-146a were identified as mediators of the 5q– syndrome phenotype (another ribosomopathy that primarily affects erythropoiesis) [18]. [score:1]
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While the exact role of each miRNA in Cluster 4, 1 and 3 is yet to be defined, it is noteworthy that miR-145, which has been implicated as an inhibitor of cell proliferation by down -regulating IGF1R in bladder cancer cells [44] and other cancers [45– 47], was present in Cluster 4. Further analysis into the functional role of each miRNA identified in these clusters is required in order to determine which miRNA have a role in developmental cardiomyocyte quiescence. [score:5]
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miR-145, miR-133a and: tumor-suppressive target FSCN1 in esophageal squamous cell carcinoma. [score:5]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-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, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-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
MiR-145 and miR-365 were specifically expressed in DRG (Fig. 3a). [score:3]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
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Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-183, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-mir-1-2, 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-10c, dre-mir-10d, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-20a, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-101a, dre-mir-101b, 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-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-mir-499, ola-mir-430a-1, ola-mir-430c-1, ola-mir-430b-1, ola-mir-430c-2, ola-mir-430c-3, ola-mir-430d-1, ola-mir-430a-2, ola-mir-430c-4, ola-mir-430d-2, ola-mir-430a-3, ola-mir-430a-4, ola-mir-430c-5, ola-mir-430d-3, ola-mir-430b-2, ola-mir-430c-6, ola-mir-430c-7, ola-mir-20a-1, ola-mir-92a-2, ola-mir-9a-2, ola-mir-101a, ola-mir-9b-1, ola-mir-499, ola-let-7a-1, ola-mir-9a-3, ola-mir-183-1, ola-let-7a-2, ola-mir-29b-1, ola-mir-29a, ola-mir-124-1, ola-mir-124-2, ola-mir-9a-4, ola-mir-101b, ola-let-7a-4, ola-mir-10d, ola-mir-9a-1, ola-mir-92b, ola-mir-9b-2, ola-mir-1-2, ola-mir-124-3, ola-mir-15a, ola-mir-10b, ola-mir-92a-1, ola-mir-20a-2, ola-mir-17, ola-mir-29b-2, ola-mir-29c, ola-mir-183-2, ola-let-7a-3, ola-mir-9a-5, ola-mir-145, dre-mir-29b3
For detailed lists of miRNA family assignments, see Supplement Table 4 The age -dependent expression of the following miRNAs was previously demonstrated by qPCR: tni-miR-15a, tni-miR-101a, tni-miR-101b, dre-miR-145, hsa-miR 29c-1 (100% identical to dre-miR-29a), hsa-let-7a-5p, hsa-miR-124a-1, hsa-miR-1-2, olamiR-21, ola-miR-183-5p and, from cluster dre-miR-17a/18a/19a, and dre-miR-20a (the used primers were Qiagen miScript primer). [score:1]
For detailed lists of miRNA family assignments, see Supplement Table 4 The age -dependent expression of the following miRNAs was previously demonstrated by qPCR: tni-miR-15a, tni-miR-101a, tni-miR-101b, dre-miR-145, hsa-miR 29c-1 (100% identical to dre-miR-29a), hsa-let-7a-5p, hsa-miR-124a-1, hsa-miR-1-2, olamiR-21, ola-miR-183-5p and, from cluster dre-miR-17a/18a/19a, and dre-miR-20a (the used primers were Qiagen miScript primer). [score:1]
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ZFIN on-line publication 83 Zeng L Carter AD Childs SJ 2009 miR-145 directs intestinal maturation in zebrafish. [score:2]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
MicroRNA-145 regulates OCT4, SOX2, and KLF4 and represses pluripotency in human embryonic stem cells. [score:1]
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