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24 publications mentioning mmu-mir-136

Open access articles that are associated with the species Mus musculus and mention the gene name mir-136. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 296
Other miRNAs from this paper: mmu-mir-200a
In comparison with the blank and NC groups, the miR-136 expression and mRNA expressions of Bax, Caspase, and E-cadherin in the miR-136 mimics and siRNA-PMEL groups significantly increased (all P<0.05), whereas the mRNA expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly decreased (all P<0.05); miR-136 expression increased markedly in the miR-136 mimics group (P<0.05), whereas no significant difference was observed in the miR-136 expression in the siRNA-PMEL group (P>0.05). [score:11]
The cells were assigned into control (subcutaneous cells from normal mice), blank (transfected with no sequence), NC (transfected with miR-136 NC), miR-136 mimics (transfected with miR-136 mimics), miR-136 inhibitors (transfected with miR-136 inhibitors), siRNA-PMEL (transfected with siRNA-PMEL), miR-136 inhibitors + siRNA-PMEL (transfected with miR-136 inhibitors and siRNA-PMEL), LiC1 (treated with Wnt signaling pathway activator) and siRNA-PMEL + LiCl groups. [score:9]
The miR-136 expression and mRNA expressions of Bax, Caspase, and E-cadherin significantly decreased in the miR-136 inhibitors group (all P<0.05), while the mRNA expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly increased (all P<0.05). [score:9]
The mRNA expressions of Bax, Caspase, and E-cadherin significantly decreased in the LiC1 group (all P<0.05), while the mRNA expressions of β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly increased (all P<0.05) and there was no significant difference in miR-136 expression and PMEL expression (P>0.05). [score:9]
A previous study showed that miR-136 had a tumor-suppressive impact on breast cancer cells by targetting PTEN, a tumor inhibitor [33]. [score:7]
The protein expressions of Bax, Caspase, and E-cadherin significantly decreased in the miR-136 inhibitors group (all P<0.05), while the protein expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly increased (all P<0.05). [score:7]
In addition, the current study also revealed that increased miR-136 expression suppressed N-cadherin, but promoted mRNA and protein expressions of E-cadherin, which were outstanding hallmarks of EMT [49]. [score:7]
MiR-136 inhibitor is a chemically modified inhibitor special to the specific target miR-136 in cells [23]. [score:7]
A significant reduction in the expression of miR-136 was observed in the miR-136 inhibitors + siRNA-PMEL group (P<0.05), whereas no significant change was observed in the mRNA expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin (all P>0.05). [score:7]
Our findings signified that PMEL expression was much higher in melanoma tissues compared with normal tissues, and miR-136 suppressed mRNA and protein expressions of PMEL. [score:6]
Collectively, the study came to a conclusion that miR-136 could attenuate cell proliferation and EMT, and stimulate apoptosis of mouse melanoma cells by targetting PMEL via down-regulation of Wnt signaling pathway. [score:6]
Figure 5The miR-136 expression and mRNA expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in each group(A) The differences in miR-136 expression amongst the four cell lines; *, P<0.05 compared with B16; (B,C) the mRNA expressions in each group after transfection; *, P<0.05 compared with the control group; [#], both P<0.05, compared with the blank group and NC group. [score:6]
The expressions of miR-136, Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in the normal group and mo del groupThe results of indicated that compared with the normal group, expressions of miR-136, Bax, Caspase, and E-cadherin significantly decreased in the mo del group, while the expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly increased (P<0.05). [score:6]
To elucidate the mechanism of miR-136 in melanoma, the present study was performed to examine the modulatory effects of miR-136 by targetting PMEL via down-regulation of Wnt signaling pathway in mouse melanoma cells. [score:6]
org was used for the target gene analysis of miR-163 and to verify if PMEL was the direct target gene of miR-136. [score:6]
In comparison with the control group, the apoptosis rate significantly and successively decreased in the blank, NC, miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL groups (all P<0.05). [score:5]
The miR-136 expression and mRNA expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in each groupThe expression of miR-136 in melanoma cell lines (B16, A375, WM239, and WM451) were evaluated by. [score:5]
Our study also showed that miR-136 inhibited the mRNA and protein expressions of β-catenin, Bcl-2, Wnt3a, and N-cadherin. [score:5]
In other groups, 250 μl serum-free Opti-MEM (51985042, Gibco, Gaitherburg, MD, U. S. A. ) was applied to dilute 100 pmol blank, NC, miR-136 mimics, miR-136 inhibitors, miR-136 inhibitors + siRNA-PMEL, and siRNA-PMEL (50 nM as the final concentration), and cells were mixed and incubated at room temperature for 5 min. [score:5]
miR-136 promoted cell apoptosis of B16 cellsIn comparison with the control group, the apoptosis rate significantly and successively decreased in the blank, NC, miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL groups (all P<0.05). [score:5]
In the mo del group, there was no obvious difference in the miR-136 expression and mRNA expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin between the blank group and NC group (P>0.05). [score:5]
After digestion, the cells in the control, blank, NC, miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL groups were washed with PBS twice. [score:5]
miR-136 inhibited cell proliferation of B16 cellsIn comparison with the control group, the OD value increased at 48 and 72 h amongst the blank, NC, miR-136 mimics, siRNA-PMEL, and miR-136 inhibitors groups (all P<0.05). [score:5]
In comparison with the control group, cell cycle distribution reduced (cell percentage decreased) in G [0]/G [1]-phase in the blank, NC, miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL groups, while the cell cycle distribution increased (cell percentage increased) in S-period (all P<0.05). [score:5]
To conclude, miR-136 decreased in melanoma, while PMEL was highly active in melanoma and consequently affected the development and progression of melanoma by regulating Wnt expression. [score:5]
In comparison with the blank and NC groups, the protein expressions of Bax, Caspase, and E-cadherin significantly increased in the miR-136 mimics group and siRNA-PMEL group (all P<0.05), while the mRNA expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly decreased (all P<0.05). [score:5]
The cell percentage in the control, blank, NC, miR-136 mimics, miR-136 inhibitors, siRNA-PMEL, and miR-136 inhibitors + siRNA-PMEL groups in G [0]/G [1]-phase was (88.70 ± 2.58)%, (70.81 ± 2.46)%, (71.79 ± 2.26)%, (80.78 ± 2.11)%, (61.52 ± 2.50)%, (79.62 ± 4.44)%, and (70.82 ± 1.33)%; and in S-phase was (1.33 ± 0.30)%, (20.95 ± 2.56)%, (22.58 ± 1.65)%, (12.96 ± 1.21)%, (31.37 ± 2.41)%, (12.82 ± 2.78)%, and (21.11 ± 1.94)%. [score:5]
There were no significant changes in the protein expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in the miR-136 inhibitors + siRNA- PMEL group (all P>0.05). [score:5]
Our current data revealed that up-expressed miR-136 inhibited melanoma cell proliferation, migration, and invasion, and stimulated apoptosis. [score:5]
The reaction conditions were as follows: predenaturation at 95°C for 30 s, followed by 40 cycles of denaturation at 95°C for 5 s, annealing at 60°C for 30 s, and extension at 72°C for 30 s. U6 was set as the internal reference for the relative expression of miR-136, and GAPDH for the relative expressions of PMEL, β-catenin, Wnt3a, Bcl-2, N-cadherin, Bax, Caspase, and E-cadherin. [score:5]
The miR-136 expression and mRNA expressions of Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in each group. [score:5]
miR-136 specifically targetted PMELAccording to the online analysis software, there is a specific binding region between the PMEL gene sequence and miR-136 sequence, therefore PMEL is one target gene of miR-136 (Figure 4A). [score:5]
Moreover, accumulated evidence showed that miR-136 served as a suppressor in the occurrence and development of various human cancers, and it may provide a therapeutic method in predicting and treating human cancers [29, 30]. [score:4]
The results of indicated that compared with the normal group, expressions of miR-136, Bax, Caspase, and E-cadherin significantly decreased in the mo del group, while the expressions of PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin significantly increased (P<0.05). [score:4]
Compared with the blank group and NC group, cell migration was significantly inhibited in the miR-136 mimics group and siRNA-PMEL group (both P<0.05), whereas it was stimulated in the miR-136 inhibitors group and LiC1 group (both P<0.05). [score:4]
Compared with the blank group and NC group, cell invasion was significantly inhibited in the miR-136 mimics group and siRNA-PMEL group (both P<0.05), while it was stimulated in the miR-136 inhibitors group and LiC1 group (both P<0.05). [score:4]
For complete understanding of the specific mechanisms of miR-136 targetting PMEL via Wnt signaling pathway, further studies are required. [score:3]
miR-136 inhibited cell migration of B16 cells. [score:3]
No significant change was observed in the miR-136 inhibitors + siRNA-PMEL group and siRNA-PMEL + LiCl group (both P>0.05) (Figure 9). [score:3]
According to the online analysis software, there is a specific binding region between the PMEL gene sequence and miR-136 sequence, therefore PMEL is one target gene of miR-136 (Figure 4A). [score:3]
miR-136 inhibited cell migration of B16 cellsThe results (Figure 8) showed that there was no evident difference in cell migration between the blank group and NC group (both P>0.05). [score:3]
The expressions of miR-136, Bax, Caspase, E-cadherin, PMEL, β-catenin, Bcl-2, Wnt3a, and N-cadherin in the normal group and mo del group. [score:3]
Quantitative real-time PCR (qRT-PCR) was performed to determine miR-136 expression in the B16, A375, WM239, and WM451 cells. [score:3]
No significant difference was observed in apoptosis rate between the miR-136 inhibitors + siRNA-PMEL, blank, and NC groups (all P>0.05) (Figure 11). [score:3]
No evident change was observed in the miR-136 inhibitors + siRNA-PMEL group and siRNA-PMEL + LiCl group (both P>0.05). [score:3]
miR-136 inhibited cell invasion of B16 cells. [score:3]
There was no significant change in OD value between the miR-136 inhibitors + siRNA-PMEL group and siRNA-PMEL+ LiCl group (both P>0.05) (Figure 7). [score:3]
The target sequence and mutant sequence were designed according to the sequence of PMEL mRNA in 3′-UTR binding to miR-136. [score:3]
Verification of targetting relationship between miR-136 and PMEL. [score:3]
The relative quantitation 2−ΔΔ C [t] method was applied to calculate the relative transcription level of target genes (miR-136, PMEL, β-catenin, Wnt3a, Bcl-2, N-cadherin, Bax, E-cadherin, and Caspase mRNA): ΔΔ C [t] = Δ C [t] (case group) – Δ C [t] (control group), Δ C [t] = C [t] (target gene) – C [t] (internal reference) [20]. [score:3]
No significant change was observed in the miR-136 inhibitors + siRNA-PMEL group and siRNA-PMEL + LiCl group (both P>0.05). [score:3]
miR-136 inhibited cell proliferation of B16 cells. [score:3]
miR-136 inhibited cell invasion of B16 cellsThere was no evident difference in cell invasion between the blank group and NC group (both P>0.05). [score:3]
Therefore, the present study was conducted to explore the modulatory effects of miR-136 on the cell proliferation, epithelial–mesenchymal transition (EMT), and apoptosis of mouse melanoma cells by targetting PMEL through Wnt signaling pathway. [score:3]
MiR-136 mimic served as a type of endogenous miRNAs, which could enhance the expression function of the endogenous miR-136 [22]. [score:3]
miR-136 specifically targetted PMEL. [score:3]
In comparison with the control group, the OD value increased at 48 and 72 h amongst the blank, NC, miR-136 mimics, siRNA-PMEL, and miR-136 inhibitors groups (all P<0.05). [score:3]
MiR-136 was expressed in melanoma cell lines with different degrees, and the B16 cells with highest expression were chosen for further investigation (P<0.05) (Figure 5). [score:2]
Thus, the identification of miR-136 down -regulating PMEL and the Wnt signaling pathway in melanoma may assist in unveiling and understanding the potential molecular mechanisms of melanoma and may aid in providing new prognostic markers for treating melanoma in the future. [score:2]
Compared with the blank group and NC group, cell cycle distribution was significantly increased (cell percentage increased) in G [0]/G [1]-phase, whereas it significantly decreased (cell percentage decreased) in S-phase in the miR-136 mimics group and siRNA-PMEL group (all P<0.05), while it evidently decreased (cell percentage decreased) in G [0]/G [1]-phase, but it significantly increased (cell percentage increased) in S-phase in the miR-136 inhibitors group and LiC1 group (both P<0.05). [score:2]
The present study showed that decreased miR-136 in mouse melanoma cells, was linked to the occurrence and development of melanoma. [score:2]
Luciferase assay was conducted to testify if PMEL was the target gene of miR-136 (Figure 4B). [score:2]
Compared with the blank group and NC group, the OD value increased in the miR-136 inhibitors group and LiC1 group at 48 and 72 h after transfection, whereas it decreased in the miR-136 mimics group and siRNA-PMEL group (all P<0.05). [score:2]
Compared with the NC group, the luciferase activity of wild-type Wt- miR-136/ PMEL was inhibited in the miR-136 mimics group (P<0.05), whereas the mutant 3′-UTR showed no significant changes (P>0.05). [score:2]
Effects of miR-136 on cell invasion of B16 cells in each group. [score:1]
Therefore, it can be concluded that miR-136 can specifically bind to the PMEL gene. [score:1]
Effects of miR-136 on cell apoptosis rate of B16 cells in each group. [score:1]
For instance, Haapa-Paananen et al. [31] investigated that miR-136 reduced in human glioma cells and stimulated cell apoptosis of glioma cells via inhibition of AEG-1 and Bcl-2 [32]. [score:1]
The expression of miR-136 in melanoma cell lines (B16, A375, WM239, and WM451) were evaluated by. [score:1]
Figure 4Verification of targetting relationship between miR-136 and PMEL(A) The predicted binding site of miR-136 on PMEL-3′-UTR; (B) luciferase activity determined by dual-luciferase reporter assay; *, P<0.05 compared with the NC group. [score:1]
Effects of miR-136 on cell cycle distribution of B16 cells in each group. [score:1]
miR-136 promoted cell apoptosis of B16 cells. [score:1]
Effects of miR-136 on cell migration of B16 cells in each group. [score:1]
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2
[+] score: 54
Expression of miR-136 was also inspected in the primary tissues and cells expressing VerUTR. [score:5]
By computational predictions, another versican-bound miRNA, miR-136, could potentially target PTEN through three binding sites on the PTEN 3′UTR (nucleotides 289–311; 490–511; and 2759–2781). [score:3]
Besides miR-144 and miR-136, two other miRNAs, miR-16 and let-7 miRNA, could potentially interact with versican 3′UTR and have hypothetical target site on the PTEN mRNA (SI Figure S5b). [score:3]
Repression on luciferase activity was removed when miR-136 targeting site was mutated. [score:3]
miR-144 and miR-136 repress PTEN translation. [score:3]
These results are summarized in Figure 6, and depict schematically that overexpression of versican 3′UTR driven by a CMV promoter could result in binding of miR-144, miR-199a-3p, and miR-136. [score:3]
The expression of miR-199a-3p and miR-136 were detected in both cells and several primary tissues but miR-144 was not found using RealTime-qPCR (results not shown). [score:3]
Computational analysis showed that miR-199a-3p, miR-144, and miR-136 potentially targeted versican 3′UTR. [score:3]
miR-136 significantly repressed luciferase activity of Luc-Pten-136, and the repression was almost abolished when the target sequence was mutated. [score:3]
miR-136 exhibitd more than one binding sites located in the 3′UTR of PTEN and the sequences of these target sites are very conserved. [score:3]
We have chosen to focus on the expression of miR-199a-3p and miR-136 because miR-144 is an erythroid lineage-specific miRNA [33]. [score:3]
Overexpression of versican 3′UTR would attract endogenous miR-199a-3p, miR-144, and miR-136. [score:3]
In addition, miR-144 and miR-136, which have also been shown to interact with versican 3′UTR, was found to target PTEN. [score:3]
In the primary lung tissues, there was a 40% significant reduction in miR-136 expression, while a significant difference between breast cancer cells transfected with VerUTR and the control vector was not detected (Figure 5c). [score:3]
Targeting of PTEN by miR-144 and miR-136. [score:3]
0013599.g006 Figure 6 Computational analysis showed that miR-199a-3p, miR-144, and miR-136 potentially targeted versican 3′UTR. [score:3]
There was no significant difference in miR-136 levels between the cells transfected with either VerUTR or the control vector. [score:1]
Similarly, there was little difference in miR-136 levels in the kidney of VerUTR transgenic and wildtype mice (Figure 5d). [score:1]
Notably, the levels of miR-199a-3p and miR-136 were consistently reduced in lung tissues but not kidney tissues. [score:1]
The abundance of miRNA was not likely the reason for this because miR-136 levels were similar in both lung and kidney (Figure 5d). [score:1]
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3
[+] score: 43
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-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, 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-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
It remains unknown whether the down-regulated miRNA* strands, miR-136-3p, -337-3p, -434-5p, -3071-3p, and -3544-5p, have regulatory roles contributing to muscle aging. [score:5]
These results suggested that Rybp and its putative regulatory miRNA, miR-136, could contribute to muscle aging process. [score:2]
miRNA Fold Change P-value mmu-miR-337-5p −5.2 0.0149 mmu-miR-3544-3p −5.1 0.0147 mmu-miR-540-5p −4.9 0.0200mmu-miR-337-3p [a] −3.0 0.0324mmu-miR-3544-5p [a] −3.0 0.0308 mmu-miR-434-3p −2.1 0.0001 mmu-miR-3071-5p −2.0 0.0004mmu-miR-136-3p [a] −2.0 0.0004mmu-miR-3071-3p [a] −1.6 0.0000 mmu-miR-136-5p −1.6 0.0000 mmu-miR-143-5p −1.2 0.0004 mmu-miR-190a-5p −1.0 0.0139 mmu-miR-872-3p −0.9 0.0152 mmu-miR-193a-3p −0.9 0.0164 mmu-miR-144-3p −0.8 0.0298 mmu-miR-127-3p −0.7 0. 0002mmu-miR-434-5p [a] −0.6 0.0082 mmu-miR-148a-3p −0.6 0.0130 mmu-miR-411-5p −0.6 0.0091 a miRNA* (passenger) strand processed from opposite arm of the mature miRNA. [score:1]
Of note, in our dataset, five miRNAs, miR-136, -337, -434, -3071, -3544, exhibited a high dominance in both the guide and passenger strands. [score:1]
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[+] score: 29
Candidate target genes regulated by the upregulated miRNAs (mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p and mmu-miR-16-1-3p). [score:7]
Of these miRNAs, four were upregulated (mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p), and one was downregulated (mmu-miR-212-3p). [score:7]
Of the five differentially expressed miRNAs, four miRNAs, namely, mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p, were significantly upregulated in the vitrified blastocysts. [score:6]
Among the upregulated miRNAs, 292, 178, 164, and 243 candidate target genes were predicted for mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p, respectively (S2 Table). [score:6]
In this study, 5 of the 760 identified miRNAs, namely, mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, mmu-miR-16-1-3p, and mmu-miR-212-3p, showed significantly different expression between the vitrified and fresh mouse blastocysts. [score:3]
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5
[+] score: 18
The combinatorial effect of ten down-regulated miRNAs (miR-144-3p, miR-33-5p, miR-32-5p, miR-1983, miR-136-5p, miR-142-3p, miR-376a-3p, miR-142-5p, miR-3968, and miR-29b-3p) reveals that a total of 61, 51, 48, and 37 target genes are significantly affected in PI3K-Akt, focal adhesion, cancer pathways, and transcriptional misregulation pathway respectively (p<0.001) (Figure 4). [score:7]
Two miRNAs miR-136-5p and miR-376a-3p down-regulated in SKH1 mice due to chronic UVR were also suppressed in wild type FVB mice skin due to UVR [13]. [score:6]
Ten miRNAs (miR-144-3p, miR-33-5p, miR-32-5p, miR-1983, miR-136-5p, miR-142-3p, miR-376a-3p, miR-142-5p, miR-3968, and miR-29b-3p) were differentially expressed (log fold change>1) and down-regulated in chronically treated SKH1 mice compared to untreated controls (Table 1-3). [score:5]
[1 to 20 of 3 sentences]
6
[+] score: 17
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Ssc-miR-136 was highly expressed in mpiPSCs but it had low expression in hpiPSCs. [score:5]
Ssc-miR-182, ssc-miR-187, ssc-miR-136, ssc-miR-210, ssc-miR-217 and ssc-miR-10b participate in regulation Neurotrophin signaling pathway by targeting corresponding genes, including BNDF, SHC4, KRAS and FOXO3. [score:4]
We also assessed another three selected miRNAs, ssc-miR-136, ssc-miR-217 and ssc-miR-182, which were found to be more highly expressed in mpiPSCs (Fig 3C). [score:3]
In the porcine Dlk1-Dio3 locus, most miRNAs were silenced except miR-136, which was highly expressed in the mpiPSCs. [score:3]
The sequencing studies only detected reads for ssc-miR-493-3p, ssc-miR-493-5p and ssc-miR-136. [score:1]
Of the miRNAs in the porcine Dik1-Dio3 region, there were four annotated miRNAs: ssc-miR-127, ssc-miR-495, ssc-miR-493 and ssc-miR-136. [score:1]
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7
[+] score: 16
Evidence of the concerted interplay of miRNAs regulated by CpG-ODN and their potential target mRNAs was observed (Fig. 4) for 2 miRNAs upregulated (hsa-miR-302b and hsa-miR-374b) and for 13 miRNAs downregulated in CpG-ODN -treated mice (hsa-miR-135a, hsa-miR-136, hsa-miR-340, hsa-miR-445-5p, hsa-miR-424, hsa-miR-96, hsa-miR-142-3p, hsa-miR-140-5p, hsa-miR-542-3p, hsa-miR-18a, hsa-miR-18b, hsa-miR-101, and hsa-miR-99a). [score:10]
Comparison of hsa-miR-18a, hsa-miR-18b, hsa-miR-140-5p, hsa-miR-101, hsa-miR-556-3p, hsa-miR-424, hsa-miR-136, hsa-miR-340, hsa-miR-302b expression obtained by miRNA expression profile and qRT-PCR on tumors collected from human IGROV-1 ovarian tumor-bearing mice treated daily i. p. with CpG-ODN or saline (control group). [score:5]
RT-qPCR using the RNA profiled in microarray analysis validated all 9 miRNAs (Fig. S1), whereas RT-qPCR using the RNA of the replica confirmed 6 of 9 miRNAs (p<0.05), with a trend observed for hsa-miR-18b and hsa-miR-101 but not for hsa-miR-136 (Fig. 2). [score:1]
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8
[+] score: 15
This corroborates our results where mmu-miR-136-5p expression levels decrease by close to 80-fold between the age of 2 days and 12 weeks in mouse quadriceps muscle. [score:3]
b Box-plots of miRNA expression levels of mmu-miR-134-5p, mmu-miR-136-5p, mmu-miR-214-3p, mmu-miR-296-5p in mouse quadriceps muscle at 2 days, 2 weeks, 4 weeks and 12 weeks after birth. [score:3]
Next-generation sequencing (NGS) technology revealed that mmu-miR-136-5p is decreased in gastrocnemius muscle from mice aged 6 and 24 months [65] and targets Rybp. [score:3]
Of interest, all 4 top-ranked miRNAs in cluster B were predicted to target one of the Pax gene family members with a high degree of certainty, potentially indicating a similar role for mmu-miR-134-5p, mmu-miR-136-5p and mmu-miR-296-5p. [score:3]
A similar array has been previously conducted in a mouse mo del of muscle regeneration [73] and several miRNAs, including mmu-miR-18a-5p, mmu-miR-136-5p, mmu-miR-31-5p and mmu-miR-199a-5p, were similarly regulated as observed in our study. [score:2]
The top-ranked miRNAs for cluster B were mmu-miR-134–5p, mmu-miR-136–5p, mmu-miR-214–3p and mmu-miR-295–5p. [score:1]
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9
[+] score: 12
Interestingly, miR-1, miR136 and miR214 inhibited SDF-1α protein expression without affecting the luciferase activity of the p-MIR-Report-SDF-1α 3′UTR. [score:5]
The gene-specific primer pairs used to amplify specific target genes were as follows, and GenBank accession numbers also be included: mmu-miR-1(NR_029528.1): GSP, 5′-GGGGTGGAATGTAAAGAAGT-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-136(AJ 459747.1): GSP, 5′-GGAACTCCATTTGTTTTGA-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-214(NR_029796.1): GSP, 5′-GACAGCAGGCACAGACA-3′ and reverse, 5′-TGCGTGTCGTGGAGTC-3′; mmu-miR-23a (NR_029740.1): GSP, 5′-CCATCACATGCCAGG-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-27a (NR_029746.1): GSP, 5′-GGGGTTCACAGTGGCTAA-3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; mmu-miR-27b(NR_029531.1): GSP, 5′-GGGGTTCACAGTGGCTAAG′ -3′ and reverse, 5′-CAGTGCGTGTCGTGGAGT-3′; U6(NM_001204274.1): forward, 5′-GCTTCGGCAGCACATATACTAAAAT-3′ and reverse, 5′-CGCTTCACGAATTTGCGTGTCAT-3′; VEGF (NC_000083.6): forward, 5′-GTCCAACTTCTGGGCTCTTCT-3′ and reverse, 5′-CCTTCTCTTCCCCTCTCT-3′. [score:2]
Because 47% of miRNA target sequences are located in the 3′UTRs of mRNAs, 47% of them in open reading frames (ORFs) and the rest in the 5′UTR [35]– [36], we speculate that miR-1, miR136 and miR214 may bind to the ORF or 5′UTR of SDF-1α, but confirmation require further investigation. [score:1]
Figure S1 The effects of miR-23a, miR-136, miR-1 and miR-214 on MSC migration. [score:1]
Lane 1, MSCs; lane 2, MSCs/cel-miR-67; lane 3, MSCs/miR-27b; lane 4, MSCs/miR-27a; lane 5, MSCs/miR-1; lane 6, MSCs/miR-23a; lane 7, MSCs/miR-136; lane 8, MSCs/miR-214. [score:1]
They were named LV-mmu-mir-1, LV-mmu-mir-136, LV-mmu-mir-214, LV-mmu-mir-23a, LV-mmu-mir-27a, LV-mmu-mir-27b, and LV-cel-mir-67 (the negative control). [score:1]
As shown in Figure 5A, miR-27b, miR-27a, miR-1, miR-136, and miR-214 reduced the level of SDF-1α protein. [score:1]
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10
[+] score: 9
Unlike miR-434 and miR-136 (PAM class C), miR-127 expression gradually decreases during the differentiation process (PAM class A), a pattern inversely correlated to that of Rtl1 expression in ES cells, as assayed by Quantitative Reverse-transcriptase PCR (Q-RT-PCR; Figure 2D). [score:4]
Among these, a short cluster of maternally expressed miRNAs genes (miR-431, miR-433, miR-127, miR-434 and miR-136) is transcribed and processed from an antisense gene to the paternally expressed Retrotransposon-like 1 (Rtl1) gene, the recently characterized protein product of which appears to be indispensable for mouse foetal development [37]. [score:4]
Our time-course analysis revealed that of these five miRNAs, only miR-127, miR-434 and miR-136, are likely to contribute to Rtl1 silencing in ES cells (Figure 2D) because their cloning frequencies largely exceeds that of the other members of the cluster, which accumulate at background level (Figure 2C, Dataset S1). [score:1]
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11
[+] score: 7
Of these, eight (miR-193b, miR-199a-3p/hsa-miR-199b-3p, miR-455-3p, miR-210, miR-381 (also known as miR-381-3p), miR-92a, miR-320c, and miR-136) were upregulated, while the other four (miR-490-5p, miR-4287, miR-BART8*, and miR-US25-1*) were downregulated during this process [22]. [score:7]
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12
[+] score: 5
Preferential expression in the retina was also observed for miR-376a, miR-138, miR-338, and miR-136 as compared with the mouse platform; it is notable, however, that these miRs are expressed at higher levels in brain than in retina. [score:4]
Indeed miR-136, miR-138, and miR-338 were previously cloned from the hippocampus and cerebral cortex [19]. [score:1]
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13
[+] score: 5
Of the latter, miR126, miR136, miR206, miR451 and miR551b showed significant, gradual down-regulation (>2 times) after birth or during development (ED16>4W>4W). [score:5]
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14
[+] score: 4
Importantly, the “transcriptional misregulation in cancer” pathway is affected by most of our differentially expressed miRNAs (miR-136-5p, miR-196a-5p, miR-196b-5p, miR-376a-3p, miR-335-5p, and miR-206-3p) significantly (p<0.001) (Figure 3A). [score:4]
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15
[+] score: 3
Other miRNAs from this paper: mmu-mir-127
Two miRNA genes, miR-127 and miR-136, have been shown to be part of an imprinted domain responsible for the imprinted expression of the retrotransposon-like gene Rtl1 in mice and the orthologous PEG11 gene in sheep and humans [93, 94]. [score:3]
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16
[+] score: 3
In the Dlk1-Dio3 region, the maternally expressed genes can produce non-coding RNAs, including mir-431, mir-433, mir-127, mir-432 and mir-136. [score:3]
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17
[+] score: 3
MiR-127 and miR-136 are reported to be processed from a transcript (antiPeg11) that is antisense to Rtl1/Peg11, a paternally expressed intronless gene [22], [23]. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
By comparing with sheep miRNA sequences, we found that 5 miRNA families containing miR-127, miR-136, miR-154, miR-229 and miR-379, were conserved in all these species It is, therefore, tempting to speculated that these 5 miRNA families are critical in mammal development. [score:2]
Other families that had a high abundance of reads were miR-134, miR-136, miR-154, miR-370, miR-412, miR-431, miR-432, miR-433, miR-485, miR-493, miR-541; a total of 11 miRNA families. [score:1]
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19
[+] score: 3
Other miRNAs from this paper: oar-mir-136
The trans-inactivation of PEG11 in CLPG/CLPG animals has been shown to result from the RISC -mediated cleavage of PEG11 mRNA by at least three perfectly complementary miRNAs (oar- miR-136, -127 and -432) processed from the maternally expressed anti-PEG11 non-coding RNA [12]. [score:3]
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20
[+] score: 2
Three microRNAs in this region, miR-431, miR-127, and miR-136, were shown previously to regulate Peg11 through a siRNA-like mechanism [52]. [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Mir-136 and mir-718 were not detectable in the adipocyte cultures using the Taqman assays-on-demand, while mir-346, mir-298, mir-330 and mir-501 were expressed at low levels (Ct levels above 33), see Table 1. This suggests that currently there is no gold standard method (when RNA is limiting) to validate miRNA data profiles. [score:2]
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22
[+] 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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
26E-0212mmu-miR-101b-3pmir-1010.297.791.72E-059.11E-0437mmu-miR-101a-3pmir-1010.2410.121.17E-031.92E-0250mmu-miR-107-3pmir-1030.228.773.24E-034.12E-0264mmu-miR-124-5pmir-1240.156.327.13E-037.09E-0233mmu-miR-301a-3pmir-1300.228.396.90E-041.29E-0259mmu-miR-130a-3pmir-1300.168.305.94E-036.44E-0252mmu-miR-135b-5pmir-1350.227.924.08E-034.99E-0274mmu-miR-136-5pmir-1360.229.061.09E-029. [score:1]
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Two miRNAs (miR-136 and miR-337) had only one significant SNP pair: for miR-136 the correspondence was found between SNPs rs37113033 (chr 19, ~5 Mb, nearest gene: Slc29a2) and rs13459176 (chr 15, ~3 Mb, nearest gene: Sepp1), while miR-337 had SNP pair rs3693942 (chr 13, ~55 Mb, nearest gene: Unc5A) and rs3663950 (chr4, ~135 Mb, nearest gene: Il22ra) (Table  2). [score:1]
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A high number of the detected miRNAs are known to play a role in stemness and differentiation, that is, let7 family, miR-125b, miR-126, miR-136, miR-143, miR-145, miR-152, suggesting that we indeed identified miRNAs that are important in reprogramming using our experimental set up. [score:1]
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