sort by

10 publications mentioning mmu-mir-665

Open access articles that are associated with the species Mus musculus and mention the gene name mir-665. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 167
Other miRNAs from this paper: mmu-mir-214
revealed that miR-665 overexpression significantly suppressed XPB1 and ORMDL3 expression levels, but miR-665 inhibition increased their expression (Figure 5b). [score:11]
Collectively, these findings indicate that upregulation of miR-665 promotes IBD progression by inactivating ER stress signaling via targeting XBP1 and ORMDL3, and miR-665 might be a potential therapeutic target. [score:8]
However, real-time PCR analysis revealed that the mRNA levels of XBP1 and ORMDL3 were not significantly changed upon alteration of miR-665 (Supplementary Figure 2), suggesting that miR-665 inhibits XBP1 and ORMDL3 expression by inducing translation repression. [score:7]
[22] In our study, miR-665 expression was markedly upregulated in experimental colitis, but antagonizing miR-665 reduces the severity of colitis. [score:6]
Expression of miRNA was defined based on the Ct, and relative expression levels were calculated as 2 [−[(Ct of miR-665)–(Ct of U6)]] after normalization with reference to the expression of U6 small nuclear RNA. [score:5]
As expected, miR-665 expression was substantially increased, with ~4–16-fold upregulation in CD (inactive CD, n=21; active CD, n=29) and UC (inactive UC, n=16; active UC, n=23) subgroups compared with normal controls, and further elevated in the patients with active colitis (Figure 1b). [score:5]
Meanwhile, we found that the accumulation of XBP1 and ORMDL3 in cellular ER was markedly reduced by overexpression of miR-665, but increased by its inhibition (Figure 5c). [score:5]
[3] Consistently, we found that ectopic expression of miR-665 increased the phosphorylation of JNK (p-JNK), while inhibition of miR-665 decreased its phosphorylation, suggesting that miR-665 promotes cell apoptosis by activating JNK (Figure 5b). [score:5]
Interestingly, using the publicly available algorithm TargetScan, we found that the core components of the UPR signaling pathway, XBP1 and ORMDL3, may be potential targets of miR-665 (Figure 5a). [score:5]
Recent evidence indicated that miR-665 was upregulated in intestinal gastric adenocarcinoma. [score:4]
[27] Interestingly, our results indicated that ectopic expression of miR-665 promoted apoptosis under different inflammatory stimuli, such as TNF- α. However, whether miR-665 might have a role in the development of CAC through the effects of inflammatory factors remains unknown. [score:4]
miR-665 is markedly upregulated in the inflamed mucosa of patients with IBD and DSS -induced colitis in mice. [score:4]
These results suggest that miR-665 directly targeted XBP1 and ORMDL3. [score:4]
[28] Interestingly, miR-665 was reported to be induced by microbiota, which in turn facilitated the infection by downregulating Abcc3 in host cells, [29] suggesting that miR-665 might be an important mediator in microbiota -induced IBD. [score:4]
Taken together, our results indicate that upregulation of miR-665 promotes inflammation -induced apoptosis in vitro. [score:4]
Thus, these results suggest that upregulation of miR-665 may contribute to IBD progression. [score:4]
Furthermore, luciferase assay showed that miR-665 overexpression attenuated the reporter activities driven by the 3′-UTRs of XPB1 and ORMDL3, whereas inhibition of miR-665 elevated these activities (Figure 5d). [score:4]
[19] In this study, we found that miR-665 was upregulated in IBD samples, and substantially repressed the components of ER stress, XBP1 and ORMDL3, leading to enhancing apoptosis by activation of JNK. [score:4]
Consistently, the cleavages of both caspase-3 and PARP were suppressed in the miR-665-silenced cells treated with DSS (Figure 3c). [score:3]
miR-665 targets ER stress components XBP1 and ORMDL3. [score:3]
[20] Although the interplay of miRNAs and ER stress response needs further investigation, we identified that miR-665 targeted to XBP1 and ORMDL3, which were in different signaling pathways of ER stress responses, then activated the expression of JNK, consequently resulting in apoptosis. [score:3]
Importantly, inhibition of miR-665 robustly impaired DSS -induced colon shortening, colitis and cell death in vivo (Figures 4b–e). [score:3]
Moreover, miR-665 expression was also increased by ~6-fold in DSS -induced colonic mucosal tissues. [score:3]
We then validated miR-665 expression in IBD tissues using real-time PCR. [score:3]
We first exogenously overexpressed miR-665 via miR-665 mimic transfection (Supplementary Figure 1). [score:3]
We observed the greatest body weight loss in mice injected with the miR-665 mimic, whereas antagomiR-665 injection significantly inhibited DSS -induced body weight loss (Figure 4a). [score:3]
Therefore, our results suggest that miR-665 may represent as a potential therapeutic target for IBD. [score:3]
By analyzing a publically published miRNA expression profile (NCBI/GEO/GSE48957; n=27, including 10 normal controls and 17 UC samples), [15] we found that miR-665 levels remained low in normal colonic mucosal biopsies but became about fourfold elevated in patients with UC (Figure 1a). [score:3]
However, ectopic expression of the miR-665 mutant did not have repressive effects on the reporter activities (Figure 5d). [score:3]
As shown in Figure 2c, the cleavages of both caspase-3 and PARP were increased in the miR-665 -overexpressing cells treated with DSS. [score:3]
On the other hand, either silencing of XBP1 or ORMDL3 promoted cellular apoptosis in miR-665 -inhibited cells (Supplementary Figure 3A–C). [score:3]
Understanding the precise role of miR-665 in IBD pathogenesis and in the ER stress response promises to increase our knowledge of the biological basis of inflammation development and may also facilitate the development of new therapeutic strategies against IBD. [score:3]
Notably, we found that miR-665 reduced XBP1 and ORMDL3 expression, and increased the activity of JNK, leading to the increased sensitivity of cellular apoptosis by inflammatory factors. [score:3]
Indeed, Annexin V and TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining assays demonstrated that ectopic expression of miR-665 increased the apoptotic rates of HT-29 and Caco-2 cells by sensitization to the chemoagent DSS (Figures 2a and b). [score:2]
Thus, miR-665 might induce a positive feedback regulation in the miR-665/ER/NF- κB loop, leading to the chronic inflammation in the gastrointestinal tract. [score:2]
We synthesized cDNA from 10 ng total RNA using a TaqMan miRNA Reverse Transcription Kit (Applied Biosystems, Foster City, CA, USA), and we quantified the expression levels of miR-665 using an miRNA-specific TaqMan MiRNA Assay Kit (Applied Biosystems). [score:2]
Moreover, a microribonucleoprotein (miRNP) immunoprecipitation (IP) assay revealed a selective association of miR-665 with XBP1 and ORMDL3 but not with GAPDH (Figure 5e), further indicating the specific effects of miR-665 on these targets. [score:2]
Notably, by analyzing the miR-665 promoter region using the CONSITE program, we found several typical NF- κB binding sites, suggesting that miR-665 might be regulated by the inflammatory NF- κB signaling pathway. [score:2]
Furthermore, we found that restoration of both XBP1 and ORMDL3 expression abrogated the stimulatory effect of miR-665 on cellular apoptosis, as indicated by Annexin V, TUNEL and colony formation assays (Figures 6d–f). [score:2]
In conclusion, our study demonstrated that miR-665 is a critical regulator of ER stress signaling, and promotes the pathogenesis in IBD. [score:2]
miR-665 sensitizes inflammation -induced apoptosis in vitro. [score:1]
We next examined the promotive effect of miR-665 on IBD in vivo, and assessed whether antagonizing miR-665 could impair DSS -induced colitis. [score:1]
Antagonizing miR-665 impairs DSS -induced colitis in vivo. [score:1]
The mice in the groups were injected intraperitoneally with 100  μl miR-665 mimic, antagomiR-665 or negative control (diluted in PBS at 2 mg/ml) three times per week for 2 weeks. [score:1]
Moreover, the effect of miR-665 on promoting apoptosis was confirmed by examining the cleavage profiles of procaspase-3 and poly (ADP-ribose) polymerase (PARP) in HT-29 and Caco-2 cells. [score:1]
We found that silencing miR-665 reduced the apoptotic rates of HT-29 and Caco-2 cells under DSS treatment (Figure 3a and b). [score:1]
Importantly, the colony formation assay indicated that miR-665 overexpression induced apoptosis of HT-29 cells in the presence of DSS, tumor necrosis factor- α (TNF- α) and lipopolysaccharide (LPS) compared with the controls (Figure 2d). [score:1]
These results suggest that miR-665 promotes DSS -induced colitis, and that antagonizing miR-665 rescues cells from these effects. [score:1]
Thus, these findings revealed that the miR-665/ER/JNK axis had an important role in IBD progression independent of p53. [score:1]
Mice were intraperitoneally injected with miR-665 mimic, antagomiR-665 or control three times a week for 2 weeks. [score:1]
Conversely, the role of miR-665 in IBD was further examined by endogenously silencing miR-665 through antagomiR-665 transfection (Supplementary Figure 1). [score:1]
Cells were co -transfected with HA-Ago1 together with 100 nM miR-665, followed by HA-Ago1 immunoprecipitation using an antibody against HA. [score:1]
XBP1 and ORMDL3 are functional effectors for miR-665 -induced apoptosis. [score:1]
Efforts need to be made to examine the crucial role of miR-665 in the progression of CAC. [score:1]
Antagonizing miR-665 impairs DSS -induced colitis in vivoWe next examined the promotive effect of miR-665 on IBD in vivo, and assessed whether antagonizing miR-665 could impair DSS -induced colitis. [score:1]
[1 to 20 of 55 sentences]
[+] score: 77
Similarly, 342 genes potentially downregulated (targets of mmu-miR-128 and mmu-miR-342-5p) and 200 potentially upregulated genes (targets of mmu-miR-465c-5p, mmu-miR-466d-3p, mmu-miR-466d-5p, mmu-miR-665, mmu-miR-683) in the colon were identified (Table S4). [score:11]
Crossing the DNA microarray-detected dysregulated genes with the potential targets of dysregulated miRNAs predicted by at least two algorithms as described above revealed a single upregulated gene, Abcc3, potentially targeted by mmu-miR-665, for the colon, whereas no overlapping gene was found for the ileum. [score:10]
Collectively, these results demonstrate that mmu-miR-665 down-regulates Abcc3 expression by directly targeting the Abcc3 3′-UTR. [score:9]
Mmu-miR-665 inhibits Abcc3 expression by directly targeting the Abcc3 mRNA 3′-UTR. [score:8]
Therefore, it is possible that microbiota upregulate Abcc3 expression by down -regulating mmu-miR-665. [score:7]
As shown in Figure 3A and B, mmu-miR-665 significantly inhibited Abcc3 expression at both mRNA and protein levels as assessed by qRT-PCR andting, respectively. [score:5]
Mmu-miR-665 is directly involved in microbiota -induced Abcc3 up-regulation. [score:5]
Bar graphs in B show the relative intensity of blots (left panel) from three independent determinations with values represent means ± S. E. M. (C, D) Mmu-miR-665 directly targets the Abcc3 mRNA 3′-UTR. [score:4]
RAW 264.7 cells were transfected with vehicle or precursors of miR-control or mmu-miR-665, and Abcc3 expression was assessed by qRT-PCR and. [score:3]
0019293.g003 Figure 3(A, B) Mmu-miR-665 represses Abcc3 expression. [score:3]
To directly examine the regulation of Abcc3 by mmu-miR-665, RAW 264.7 cells were transfected with vehicle, or a mmu-miR-665 precursor, or a control miRNA precursor. [score:3]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers: For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′ mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression: Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′; Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
We then sought to investigate if mmu-miR-665 directly targets the 3′-UTR of Abcc3 mRNA. [score:2]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers:For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression:Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′;Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
Mmu-miR-665 significantly repressed luciferase activity (Figure 3C) and GFP production (Figure 3D) in these cells, whereas vehicle or miR-control did not exhibit any significant effect. [score:1]
RAW 264.7 cells were transfected with a luciferase or a GFP vector containing the Abcc3 3′-UTR in the presence or absence of mmu-miR-665. [score:1]
RAW 264.7 cells were then transfected with Abcc3-luc or Abcc3-GFP constructs together with vehicle or mmu-miR-665 or miRNA-control. [score:1]
[1 to 20 of 17 sentences]
[+] score: 23
Other miRNAs from this paper: mmu-mir-185, mmu-mir-882
To test this hypothesis, we selected five protein-coding genes (Bcl2, Ill7rd, Pnpla3, Shisa7 and Tapbp;1) whose expression was significantly down-regulated by reduced expression of Pbcas4 and whose mouse and human protein-coding gene orthologous pairs are both predicted to have miR-185/882 and miR-665 MREs in their 3' UTRs. [score:8]
Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely (1.7-fold increase, P < 0.02, Fisher's exact test; Figure 3b) to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. [score:8]
The percentage of genes that have a conserved (mouse and human) MRE for either miR-185/882 or miR-665 (Y-axis) is 33% and 58% for genes up- and down-regulated, respectively, upon Pbcas4 knockdown. [score:5]
We chose not to test miR-665 since, unlike miR-185, its mature sequence differs, by a single nucleotide, in human and mouse. [score:1]
Of the 12 MREs predicted in the full-length Pbcas4 transcript in N2A cells, 2 (miR-185/882 and miR-665) are also predicted to bind the human orthologous BCAS4 3' UTR. [score:1]
[1 to 20 of 5 sentences]
[+] score: 14
Our contention was supported by several findings: (1) MCF-7-miR665 cells exhibited 8–10 fold upregulation of TGFβ-R2 relative to MCF-7 cells (Fig.   7A), rather than miR655 mediated downregulation of TGFβ-R2 as noted by Harazano et al. [43]. [score:7]
By differential gene and miRNA microarray analyses of MCF7 and ectopic COX-2 over -expressing MCF-7-COX-2 cells we identified two COX-2 upregulated miRNAs, miR526b and miR665, of which miR526b was established as an oncogenic miRNA in human breast cancer [37]. [score:6]
In contrast MCF7-miR665 cells exhibited no change in Smad-3 phosphorylation or in morphology when treated with TGF-β1 (Fig.   7C,D). [score:1]
[1 to 20 of 3 sentences]
[+] score: 8
Finally, the remaining 24 miRNA exhibited differential expression between tumor and parenchyma in both the absence and presence of cigarette smoke exposure, including 2 miRNA (mmu-miR-135b-5p, mmu-miR-1198-5p), whose expression levels increased in parenchyma but remained stable in tumor tissue following MS exposure, 5 miRNA (mmu-miR-21-5p, mmu-miR-31-5p, mmu-miR-146b-5p, mmu-miR-665-3p, mmu-miR-744-5p) that remained more highly expressed in tumors compared to parenchyma, and 17 miRNA with lower expression levels in tumors than in parenchyma, even upon cigarette smoke exposure (Figure 8). [score:8]
[1 to 20 of 1 sentences]
[+] score: 7
ZFP488 is a transcription factor involved in oligodendrocyte differentiation and is targeted by four estrogen -downregulated miRNAs (miR-93-5p, miR-217-3p, miR-665-5p, and miR-3072-5p) [68]. [score:6]
Several of these miRNAs (mir-299, mir-431, mir-467c, mir-222, mir-32, mir-330, mir-384, mir-665, and mir-671) have previously been identified as sex-biased in the neonatal mouse whole brain and/or rat cortex [23, 48]. [score:1]
[1 to 20 of 2 sentences]
[+] score: 5
Propofol -induced rno-miR-665 targets BCL2L1 and influences apoptosis in rodent developing hippocampal astrocytes. [score:3]
Rno-miR-665 is involved in the neurotoxicity induced by propofol via a caspase-3, through negative regulation of BCL2L1 (Sun et al., 2015). [score:2]
[1 to 20 of 2 sentences]
[+] score: 3
ADAM10 is the target of miR-665 [11]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
WT) Musmusculus mmu-miR-205_st 0.0031763 –11.649 Musmusculus mmu-miR-200c_st 0.0246158 –3.802 Musmusculus mmu-miR-184_st 0.0170031 –3.06739 Musmusculus mmu-miR-431_st 0.00570439 –2.43854 Musmusculus mmu-miR-669e_st 0.00155807 –2.42538 Musmusculus mmu-miR-3470a_st 0.00672318 –1.97946 Musmusculus mmu-miR-491_st 0.00328488 –1.94599 Musmusculus mmu-miR-3064-5p_st 0.0276855 –1.77619 Musmusculus mmu-miR-466f_st 0.00409442 –1.75841 Musmusculus mmu-miR-2182_st 0.00532508 –1.70938 Musmusculus mmu-miR-341_st 0.0497367 –1.70718 Musmusculus mmu-miR-665-star_st 0.00544338 –1.69474 Musmusculus mmu-miR-1943-star_st 0.0157678 –1.64527 Musmusculus mmu-miR-486_st 0.0396356 –1.63793 Musmusculus mmu-miR-467a-star_st 0.00240509 –1.60868 Musmusculus mmu-miR-669f-5p_st 0.0107809 –1. [score:1]
[1 to 20 of 1 sentences]
[+] score: 1
org/microrna/) Meg3mmu-miR-770 # Bmp1, Bmp15, Capn3, Casq2, Fosb, Lmna, Mb, Obscn, Peg10, Ppp1ca, Sspn, Tmod1, Trp53 Unidentified mmu-miR-673 Camk2a, Camk2b, Camk2d, Camk2g, Dnmt1, Mtpn, Myh6, Ndn, Pax3, Rbl1, Sln, Tnnt1, Wnt1 Unidentifiedmmu-miR-493 # Cacng5, Camk2g, Cdkn1c, Ctcf, Dag1, Fhl1, Fos, Hras1, Jun, Mib2, Mtap, Peg10, Shh, Tmod1 Unidentifiedmmu-miR-337 # Capza2, Des, Dmd, Dnmt3a, Myh8, Mypn, Nfatc1, Plagl2, Pvalb, Sgcb, Snta1, Tpm3, Trp53 Unidentified mmu-miR-540 Akt3, Bmp2, Bmp7, Capzb, Emd, Itga7, Itgb1, Msc, Myog, Nkx2-5, Pten, Rhoa, Sln, Tlx1, Vim Unidentifiedmmu-miR-665 # Casq2, Igf2, Junb, Ldb3, Peg10, Magel2, Nnat, Pax3, Ryr1, Sntb2, Tln1, Tpm2, Trp53, TtnAnti-Peg11 $ mmu-miR-431 # d Camk2b, Casq1, Dtna, E2f1, Fgf4, Gata3, Igf1, Kit, Max, Peg10, Plagl2, Ppp3r1, Sgcd, Tcf21Anti-Peg11 $ mmu-miR-433 # Bmpr1b, Capza1, Creb1, Ctcf, E2f3, Gata6, Isl1, Jak2, Myh9, Peg10, Plagl2, Ppp3r1, Sntg1Anti-Peg11 $ mmu-miR-127 # d e Auts2, Bcl6, Camk2d, Cdc42, Creb5, E2f3, Igf2, Myo1c, Otx1, Plagl2, Pitx2. [score:1]
[1 to 20 of 1 sentences]