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24 publications mentioning mmu-mir-216b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-216b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 96
Our in silico analysis revealed that miR-216 and miR-217 potentially target many important genes that play critical roles during the pathogenesis of PC (Table 1); and the downregulation of miR-217 [45] and miR-216 [44] suggests their potential as tumor suppressors in PC by targeting downstream targets, particularly the Kras oncogene [43] and Janus kinase 2 [44]. [score:12]
At 30 weeks of age, the expression of miR-216 (p-value = 0.016), miR-217 (p-value = 0.0078), miR-150 (p-value =0.023), Let-7b (p-value = 0.031,) and miR-96 were significantly downregulated, whereas the expression of miR-146b (p-value = 0.0078), miR-205, (p-value - 0.0078), miR-21, miR-195 (p-value = 0.031), and miR-34c (p-value = 0.063) were significantly upregulated in KC animals compared to control animals (Figure 2B). [score:10]
The expression of miR-223, miR-483-3p (p-value = 0.01), 146b, 205 (p-value = 0.001), 221, 21 (p-value = 0.023), 195, 34c and miR-26a (p-value = 0.0078) were significantly upregulated, whereas the expression of miR-216, miR-141, miR-217, Let-7b (p-value = 0.001), and Let-150 (p-value = 0.01) were significantly downregulated in human PC tissues as compared to the cancer-adjacent normal tissues (Figure 3E). [score:10]
At 40 weeks of age, the expression of miR-216, miR-217, miR-223, miR-141, miR-483-3p (p-value = 0.031), miR-195, Let-7b (p-value = 0.063) and miR-96 were significantly downregulated; on the other hand, the expression of miR-21, miR-205, miR-146b (p-value = 0.031), and miR-34c (p-value = 0.063) were upregulated in KC mice compared to the control animals (Figure 2C). [score:10]
The panel of differentially expressed miRNAs were validated by real-time PCR using TaqMan assays, and the results were consistent with the data that showed up-regulation of miR-21, miR-221, miR-100 and miR-26a and down-regulation of miR-26b, miR-141, miR-96, miR483-3p, miR-216, and miR-217 in the KC compared to control mice (Figure 1A). [score:7]
In addition to KC mice, we also observed a significant downregulation of miR-216 and miR-217 in human PC tissue (Figure 3E); these results are in agreement with earlier studies on human PC [38– 43] that show downregulation of miR-217 in 76.2% (16/21) of PC tissue as well as cell lines [43]. [score:7]
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
Similarly, the expression of miR-216 is significantly downregulated in PC [44]. [score:6]
Several studies have shown the abnormal expression of miRNAs including miR-21, Let-7b, miR-100, miR-217, and miR-216 in PC and have proposed them as candidates for early diagnosis and potential molecular targets [23, 24]. [score:5]
The expressions of miR-216 and miR-217 were also progressively reduced in KC mice, but the expressions of miR-21, miR-205, miR-146b, miR-34c, and miR-223 progressively increased (Figure 1A, 2A– 2D). [score:5]
The expression of pancreas-specific tumor suppressors miR-217 and miR-216 were unaltered at 10 weeks of age (presence of PanIN-Ia and Ib), but progressively decreased from 25 – 50 weeks of age as PanIN lesions progressed to PDAC. [score:5]
Both miR-216 and miR-217 act as potential tumor suppressors for PC by targeting the Kras oncogene [43]. [score:5]
Further, at 50 weeks of age, the expression of miR-216, miR-217, miR-345, miR-141, miR-483-3p, miR-26b, miR-96, Let-7b (p-value = 0.01), miR-100, miR-26a and miR-150 (p-value = 0.094) were further downregulated in KC animals compared to control mice (Figure 2D). [score:5]
On the other hand, miR-146b, miR-34c, miR-223, miR-195 (p-value = 0.031) and miR-216 (p-value = 0.063) were downregulated in KC mice compared to control littermates. [score:3]
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2
[+] score: 79
Mechanically, histamine upregulates the expression of miR-206 and miR-216b via histamine 1 receptor, which act together to downregulate autophagy-related gene 13 (Atg13) expression, leading to the diminution of autophagy activity and caspase-8 activation. [score:11]
Knockdown of miR-206 and miR-216b simultaneously could raise Atg13 expression reduced by histamine under hypoxia, whereas overexpression of miR-206/216b cut down Atg13 level (Fig.   6g). [score:6]
Histamine increases miR-206 and miR-216b expression, which work combined to downregulate Atg13, resulting in the reduction of autophagy. [score:6]
We used chemically modified antisense oligonucleotides (Antagomir, Anta) to inhibit miR-206 and miR-216b expression. [score:5]
We consequently used TargetScan to analyze the potential targets of miR-206 and miR-216b in autophagy. [score:5]
But knockdown of miR-206 and miR-216b (miR-206/216b) simultaneously remarkablely abolished the suppression of histamine on the formation of LC3II, the degradation of p62 (Fig.   5b; Supplementary Figure  3c), the punctate accumulations of GFP-LC3 (Fig.   5c) and apoptosis (Fig.   5d) under hypoxia. [score:4]
Pyrilamine reduced the levels of miR-206 and miR-216b upregulated by histamine (Fig.   5e). [score:4]
To confirm whether Atg13 is really a direct target of miR-206 or miR-216b, we created the luciferase constructs with a wildtype Atg13 3′-UTR (Atg13-WT-3′-UTR), with a miR-206 -binding site-mutated Atg13 3′-UTR (Atg13-MUT1-3′-UTR), with a miR-216b -binding site-mutated Atg13 3′-UTR (Atg13-MUT2-3′-UTR) or with two binding sites-mutated Atg13 3′-UTR (Atg13-MUT1/2–3′UTR) (Fig.   6b). [score:4]
a miR-206 and miR-216b harbored conserved targeting sites in Atg13 3′-UTR. [score:3]
Fig. 6 a miR-206 and miR-216b harbored conserved targeting sites in Atg13 3′-UTR. [score:3]
These data suggested Atg13 as a co-target gene of miR-206 and miR-216b acting in concert. [score:3]
One of them alone could not recreate histamine autophagic effect or influence the protein level of Atg13, implying miR-206 and miR-216b act in concert to repress the translation of Atg13. [score:3]
Unexpectedly, miR-206 or miR-216b alone has no significant effect on the level of Atg13 protein (Supplementary Figure  4c and 4d), whereas miR-206/216b mixture remarkablely subdued the translation of Atg13 (Fig.   6e). [score:3]
MiR-206 and miR-216b jointly target to Atg13. [score:3]
MiR-206 and miR-216b mimics were transfected into H9c2 cells to increase their levels up to 10 [−5] M histamine induced (Supplementary Figure  3e). [score:1]
c H9c2 cells were transfected with GFP-LC3 accompanied by miR-206 and miR-216b antagomirs (miR-206/216b Anta) or negative controls (Anta-NC). [score:1]
Histamine repressed the activity of luciferase constructs of Atg13-WT-3′-UTR under hypoxia, and this was attenuated by miR-206 and miR-216b antagomir co-transfection (Fig.   6d). [score:1]
In addition, the absolute quantification of miR-206 and miR-216b in cardiomyocytes confirmed their increases upon histamine treatment (Supplementary Figure  3d). [score:1]
b Luciferase constructs of wildtype Atg13 3′-UTR (Atg13-WT-3′-UTR), mutated Atg13 3′-UTR in the miR-206 -binding site (Atg13-MUT1-3′-UTR), mutated Atg13 3′-UTR in the miR-216b -binding site (Atg13-MUT2-3′-UTR), and mutated Atg13 3′-UTR in the miR-206/216b binding sites (Atg13-MUT1/2–3′UTR) are shown. [score:1]
Our data showed histamine increased miR-206 and miR-216b simultaneously. [score:1]
These data demonstrate that both miR-206 and miR-216b were the essential mediators of histamine functioning on myocardial autophagy. [score:1]
Interestingly, we noticed that both miR-206 and miR-216b possessed conserved binding sites on 3′-UTR of Atg13 (Fig.   6a). [score:1]
The role of miR-206 and miR-216b in histamine signaling was further confirmed in vivo. [score:1]
After 12 h, miR-206 and miR-216b mimics mixture (miR-206/216b mimics) were transfected into cells for another 12 h. LC3 and p62 were analyzed by western blotting. [score:1]
e Cells were treated with 10 μM Histamine with 1 μM H1R antagonist (pyrilamine) or 50 μM H2R antagonist (cimetidine) for 12 h. The levels of miR-206 and miR-216b were determined by RT-PCR. [score:1]
Next, we infected cells with adenovirus harboring Atg13 with wildtype 3′-UTR along with miR-206, miR-216b, miR-206/216b mixture, or negative control. [score:1]
The results revealed the levels of miR-206, miR-30e, miR-216b, miR-133a, and miR-212 exhibited the top five significant changes upon histamine treatment, among which miR-206, miR-30e, miR-216b, and miR-133a increased, whereas miR-212 decreased (Fig.   5a; Supplementary Figure  3a). [score:1]
b H9c2 cells were transfected with miR-206 and miR-216b antagomirs together (miR-206/216b Anta) or negative controls (Anta-NC) for 8 h and then treated with 10 μM histamine under hypoxia for 12 h. LC3 and p62 were analyzed by western blotting at 3d after surgery. [score:1]
Deletion of miR-206 and miR-216b simultaneously could attenuate the prohibitive effect of histamine on Atg13 level, LC3II formation (Fig.   6j; Supplementary Figure  4e), and cell death (Fig.   6k), as well as abolished the protective effect of histamine on myocardial function in response to MI in HDC [−/−] mice (Fig.   6l). [score:1]
Histamine increases miR-206 and miR-216b to repress hypoxia -induced autophagy. [score:1]
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3
[+] score: 36
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
miR-21a-3p, miR-31-5p, miR-155-5p and miR-200c were upregulated while miR-217-5p, miR-802-5p, miR-375-5p and miR-216-5p were downregulated (Color figure online) Surprisingly, in upregulated mRNAs, it was not the classical pancreatic progenitor-related genes that changed the most. [score:10]
In our results, miR-21a, miR-31, miR-200c and miR-155 were upregulated and miR-217, miR-802, miR-375 and miR-216 were downregulated (Additional file 9: Table S5). [score:7]
In downregulated miRNAs, miR-216a-3p/5p, miR-216b-3p/5p, miR-217-5p, miR-802-3p/5p and miR-375-3p lay on the top. [score:4]
AC Azevedo-Pouly, DS Sutaria, J Jiang, OA Elgamal, F Amari, D Allard, et al. miR-216 and miR-217 expression is reduced in transgenic mouse mo dels of pancreatic adenocarcinoma, knockout of miR-216/miR-217 host gene is embryonic lethal. [score:4]
miR-216/miR-217 were supposed to be reduced in pancreatic adenocarcinoma [37]. [score:1]
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4
[+] score: 16
For example, Hlf was targeted by mmu-miR-18b-5p, mmu-miR-429-3p and mmu-miR-291a-3p; Cnot6 and Zfp91 were targeted by mmu-miR-206-3p and mmu-miR-291a-3p; Rbfox2 was targeted by mmu-miR-429-3p and mmu-miR-449c-5p; Aebp2 was targeted by mmu-miR-125a-3p, mmu-miR-223-3p and mmu-miR-496-3p; Nfya was targeted by mmu-miR-199a-5p, mmu-miR-216b-5p and mmu-miR-671-5p; Nucks1 was targeted by mmu-miR-142-3p, mmu-miR-146a-5p and mmu-miR-223-3p; Notch2 was targeted by mmu-miR-146a-5p and indirectly via Ascl1 by mmu-miR-1903. [score:16]
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5
[+] score: 11
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-136, 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-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-216 and ssc-miR-217 were also located in the same genome loci in chromosome 3. Overexpression of has-miR-216a/217 activates the PI3K/Akt and TGF-β signaling pathways by targeting PTEN and SMAD7 in human hepatocellular carcinoma cells [54]. [score:5]
Additionally, ssc-miR-216, ssc-miR-217, ssc-miR-142-5p, ssc-miR-96-5p, ssc-miR-182 and ssc-miR-183 have higher expression levels in mpiPSCs than that in hpiPSCs (Fig 3A). [score:3]
Ssc-miR-216 was also highly expressed in mpiPSCs. [score:3]
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6
[+] score: 8
In experimental diabetic nephropathy mo dels, TGF-β and miR-192 upregulate miR-216 and 217, which in turn inhibit their target molecule, Pten, resulting in Akt activation, survival and hypertrophy of glomerular mesangial cells [14]. [score:8]
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7
[+] score: 7
In addition, miR-216b suppresses the proliferation and invasion via inhibiting KRAS expression [19]. [score:7]
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8
[+] score: 7
Other miRNAs from this paper: mmu-mir-126a, mmu-mir-216a, mmu-mir-216c, mmu-mir-126b
We previous reported that CCN1 promotes VEGF-A expression in osteoblasts and subsequently enhances angiogenesis through the inhibition of miR-216 during RA disease [20]. [score:7]
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9
[+] score: 6
Last hsa-miR-216 was upregulated in cancer patients as compared to patients diagnosed with pancreatitis, with sensitivity of 50% and specificity of 100%. [score:3]
We found that salivary hsa-miR-216 may help discriminate pancreatitis from PDAC, with excellent specificity (100%), but poor sensitivity (50%) (Table 3). [score:1]
In this pilot study, we found that four salivary miRNAs (hsa-miR-21, hsa-miR-23a, hsa-miR-23b and hsa-miR-29c) successfully segregated PDAC patients from cancer-free donors, while hsa-miR-210 and let-7c indicate pancreatitis and hsa-miR-216 discriminates pancreatitis from cancer. [score:1]
However, at this stage of this project, salivary testing failed to differentiate between pancreatitis and PDAC, as hsa-miR-216 is detected only in pancreatitis and not in cancer, but with poor sensitivity. [score:1]
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10
[+] score: 6
MiR-186, miR-216b, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting α subunit of protein kinase CKII in human colorectal cancer cells. [score:3]
For example, it is known that human miR-186-5p, miR-216b-5p, miR-337-3p, and miR-760 cooperatively induce cellular senescence by targeting the gene CSNK2A1 in human colorectal cancer cells [35]. [score:3]
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11
[+] score: 6
Importantly, other downregulated miRNAs with key roles in tumorigenesis such as miR-216b, which targets K-RAS oncogene in nasopharyngeal carcinoma and colorectal cells, were identified 13 14. [score:6]
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12
[+] score: 5
Recently, miRNA expression profiles [19] revealed that several miRNAs (miR-192, miR-194, miR-204, miR-215, and miR-216) are highly and nearly exclusively expressed in the kidney. [score:5]
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13
[+] score: 5
Recent studies have suggested important regulatory roles for miRNAs such as miR-21, miR-216, miR-217, miR-181b, miR-31b and miR-34a, which were confirmed to be upregulated in senescing HUVECs (Menghini et al., 2009), and miR-146, miR-142-3p, miR-223 and miR-29 family members, which were significantly increased in whole aortas of aged mice (Zhao et al., 2010). [score:5]
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14
[+] score: 4
MiR-216b-5p was increased in 1 vehicle treated animal and miR-217-5p was increased in 2 vehicle treated animals with no histopathologic or clinical chemistry correlates (data not shown). [score:1]
In 3 μg/kg treated dogs miR-216b-5p and miR-141-3p were increased at some time points, but miR-216b-5p was not increased beyond the level of the vehicle treated dog and did not display consistent time dependent increases. [score:1]
MiR-216b-5p reached levels as high as 649 fold above vehicle in individual animals and remained elevated until 24 h. The remaining miRNAs did increase and remained elevated generally as long, but not to the degree of miRs-216a-5p and 216b-5p. [score:1]
MiR-216b displayed similar kinetics to miR-216a-5p, but with a reduced dynamic range while miR-217-5p displayed increases similar to amylase. [score:1]
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15
[+] score: 4
Accumulation of the DDIT3 -dependent micro -RNA, miR-216b, has been found to directly target JUN [49]. [score:4]
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16
[+] score: 3
Previous studies have reported that miR-216a, miR-216b, and miR-217 are specifically expressed in the pancreas; these miRNAs were useful as biomarkers for pancreatic injury [30]. [score:3]
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17
[+] score: 3
In the past few years, a number of studies of miRNAs in AD have emerged to support that deregulated miRNAs, such as miR-18b, miR-34c, miR-615, miR-211, miR-216 and miR-325, play important roles in the development and prognosis of AD [16]. [score:3]
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18
[+] score: 3
Among the known ~2,500 miRNA by deep sequencing of human genome [12], miR-192, miR-194, miR-204, miR-215 and miR-216 are highly expressed in kidney than other human tissues [13]. [score:3]
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19
[+] score: 2
Other miRNAs from this paper: mmu-mir-146a, mmu-mir-34c, mmu-mir-532
Up to now, only miR-532-3p, miR-216b, miR-34c and miR-146a were identified as potential regulators of cardiac complications of doxorubicin [17]. [score:2]
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20
[+] score: 2
Other miRNAs from this paper: hsa-mir-216a, mmu-mir-216a, hsa-mir-216b, mmu-mir-216c
Quantitative data suggested that the JAK2 expression in GC tissues with high miR-216 level was significantly decreased compared with those with low miR-216a level (P<0.05, Figure 5F). [score:2]
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21
[+] 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-21, hsa-mir-22, hsa-mir-25, hsa-mir-33a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-141, mmu-mir-155, mmu-mir-10b, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-183, mmu-mir-184, hsa-mir-192, mmu-mir-200b, hsa-mir-129-1, mmu-mir-122, 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-183, hsa-mir-210, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-129-2, hsa-mir-184, 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-21a, mmu-mir-22, mmu-mir-96, mmu-mir-34a, mmu-mir-129-2, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-25, mmu-mir-210, mmu-mir-181a-1, mmu-mir-216a, mmu-mir-223, mmu-mir-33, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, mmu-mir-217, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-375, mmu-mir-375, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-33b, hsa-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, mmu-mir-216c, bbe-let-7a-1, bbe-let-7a-2, bbe-mir-10a, bbe-mir-10b, bbe-mir-10c, bbe-mir-125a, bbe-mir-125b, bbe-mir-129a, bbe-mir-129b, bbe-mir-133, bbe-mir-1, bbe-mir-183, bbe-mir-184, bbe-mir-200a, bbe-mir-200b, bbe-mir-210, bbe-mir-216, bbe-mir-217, bbe-mir-22, bbe-mir-252a, bbe-mir-252b, bbe-mir-278, bbe-mir-281, bbe-mir-33-1, bbe-mir-33-2, bbe-mir-34a, bbe-mir-34b, bbe-mir-34c, bbe-mir-34d, bbe-mir-34f, bbe-mir-375, bbe-mir-7, bbe-mir-71, bbe-mir-9, bbe-mir-96, bbe-mir-34g, bbe-mir-34h, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In contrast, many phylogenetically conserved miRNAs, as well as miRNAs present in both chordates and vertebrates (for example, miR-216, miR-217, miR-22, miR-25, and miR-96), could be reliably traced back to B. belcheri (Gray). [score:1]
Based on the available nematode, fruitfly, zebrafish, frog, chicken, mouse, rat and human miRNA information [18], 45 conserved amphioxus miRNAs could be classified into three distinct groups: 23 miRNAs (let-7a, miR-1, miR-7, miR-9, and so on) were conserved throughout the Bilateria; 5 miRNAs (miR-252a, miR-252b, miR-278, miR-281 and miR-71) were homologous to invertebrate miRNAs; and 17 miRNAs (miR-141, miR-200a, miR-200b, miR-183, miR-216, miR-217, miR-25, miR-22, miR-96, and so on) were present both in chordates and vertebrates (Table S9 in). [score:1]
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22
[+] score: 2
Previous study reported that miR-216 and miR-217 promoted TGF β -induced MC hypertrophy in vitro by regulating PTEN 32. [score:2]
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23
[+] score: 1
These are mir-17, mir-22, mir-28, mir-32, mir-128b, mir-135b, mir-143, mir-151, mir-181b-2, mir-205, mir-213, mir-216 and mir-372. [score:1]
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24
[+] score: 1
However, ISH detection of other retina-specific miRs, including miR-213, miR-216, and miR-217, was unsuccessful in retina [26, 27]. [score:1]
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