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miRBase |
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![]() 15 publications mentioning mmu-mir-216cOpen access articles that are associated with the species Mus musculus and mention the gene name mir-216c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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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-26a-1, hsa-mir-26b, hsa-mir-31, hsa-mir-96, hsa-mir-100, mmu-let-7g, mmu-let-7i, mmu-mir-138-2, mmu-mir-141, mmu-mir-150, mmu-mir-155, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-195a, mmu-mir-200b, mmu-mir-205, hsa-mir-148a, hsa-mir-10a, hsa-mir-10b, hsa-mir-199b, hsa-mir-205, hsa-mir-216a, hsa-mir-217, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-138-2, hsa-mir-141, hsa-mir-138-1, hsa-mir-150, hsa-mir-194-1, hsa-mir-195, mmu-mir-148a, 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-26a-1, mmu-mir-26b, mmu-mir-31, mmu-mir-96, mmu-mir-345, hsa-mir-200c, hsa-mir-155, mmu-mir-10a, mmu-mir-100, mmu-mir-200c, mmu-mir-216a, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-199b, mmu-mir-138-1, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-375, hsa-mir-379, mmu-mir-375, mmu-mir-379, hsa-mir-345, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, hsa-mir-483, hsa-mir-146b, hsa-mir-494, mmu-mir-483, mmu-mir-541, mmu-mir-494, mmu-mir-216b, mmu-mir-146b, hsa-mir-541, hsa-mir-216b, hsa-mir-451b, mmu-mir-195b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k
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).
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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.
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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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Other miRNAs from this paper: mmu-mir-29b-1, mmu-mir-155, mmu-mir-21a, mmu-mir-26a-1, mmu-mir-31, mmu-mir-200c, mmu-mir-216a, mmu-mir-26a-2, mmu-mir-29b-2, mmu-mir-217, mmu-mir-375, mmu-mir-216b, mmu-mir-802, mmu-mir-21b, mmu-mir-21c
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]
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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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-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-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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Other miRNAs from this paper: mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-155, mmu-mir-200b, mmu-mir-206, mmu-mir-30e, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-192, mmu-mir-200a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-200c, mmu-mir-216a, mmu-mir-29b-2, mmu-mir-217, mmu-mir-216b, mmu-mir-21b, mmu-mir-21c, mmu-mir-30f
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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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].
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Other miRNAs from this paper: hsa-let-7c, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-31, mmu-mir-23b, hsa-mir-210, hsa-mir-216a, hsa-mir-23b, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-29c, mmu-mir-31, mmu-mir-17, mmu-mir-210, mmu-mir-216a, hsa-mir-29c, mmu-mir-216b, hsa-mir-216b, hsa-mir-940, hsa-mir-3679, mmu-mir-21b, mmu-mir-21c
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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Other miRNAs from this paper: mmu-mir-194-1, mmu-mir-200b, mmu-mir-204, mmu-mir-192, mmu-mir-200a, mmu-mir-21a, mmu-mir-29c, mmu-mir-200c, mmu-mir-216a, mmu-mir-194-2, mmu-mir-215, mmu-mir-216b, mmu-mir-21b, mmu-mir-21c
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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Other miRNAs from this paper: mmu-mir-29b-1, mmu-mir-125a, mmu-mir-142a, mmu-mir-146a, mmu-mir-34c, mmu-mir-34b, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-216a, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-29b-2, mmu-mir-181b-1, mmu-mir-217, mmu-mir-181b-2, mmu-mir-216b, mmu-mir-146b, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b
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).
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Other miRNAs from this paper: mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-201, mmu-mir-291a, mmu-mir-296, mmu-mir-34c, mmu-mir-26b, mmu-mir-325, mmu-mir-135b, mmu-mir-32, mmu-mir-200c, mmu-mir-216a, mmu-mir-211, mmu-mir-135a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-377, mmu-mir-196b, mmu-mir-470, mmu-mir-369, mmu-mir-216b, mmu-mir-708, mmu-mir-713, mmu-mir-615, mmu-mir-190b, mmu-mir-18b, mmu-mir-297c, mmu-mir-1190, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-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].
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Other miRNAs from this paper: mmu-mir-194-1, mmu-mir-204, mmu-mir-192, mmu-mir-216a, mmu-mir-194-2, mmu-mir-215, mmu-mir-216b
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].
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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).
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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, mmu-mir-216b, hsa-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, 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).
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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).
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Other miRNAs from this paper: mmu-mir-130a, hsa-mir-196a-1, hsa-mir-196a-2, hsa-mir-214, hsa-mir-216a, hsa-mir-217, mmu-mir-130b, hsa-mir-130a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-214, mmu-mir-216a, mmu-mir-217, hsa-mir-130b, mmu-mir-216b, hsa-mir-216b, mmu-mir-130c
Previous study reported that miR-216 and miR-217 promoted TGF β -induced MC hypertrophy in vitro by regulating PTEN 32.
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Other miRNAs from this paper: mmu-mir-15b, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-140, mmu-mir-151, mmu-mir-152, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-205, mmu-mir-143, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-22, mmu-mir-24-2, mmu-mir-26b, mmu-mir-29a, mmu-mir-27a, mmu-mir-93, mmu-mir-34a, mmu-mir-323, mmu-mir-325, mmu-mir-346, mmu-mir-135b, mmu-mir-107, mmu-mir-17, mmu-mir-28a, mmu-mir-32, mmu-mir-216a, mmu-mir-218-2, mmu-mir-223, mmu-mir-221, mmu-mir-222, mmu-mir-135a-2, mmu-mir-181c, mmu-mir-194-2, mmu-mir-133a-2, mmu-mir-181b-2, mmu-mir-215, mmu-mir-196b, mmu-mir-370, mmu-mir-367, mmu-mir-301b, mmu-mir-216b, mmu-mir-193b, mmu-mir-28c, mmu-mir-28b
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.
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Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-124-3, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-146a, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-184, mmu-mir-204, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, 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-23a, mmu-mir-26b, mmu-mir-29c, mmu-mir-31, mmu-mir-96, mmu-mir-129-2, mmu-mir-338, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-216a, 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, mmu-mir-217, mmu-mir-376a, mmu-mir-335, mmu-mir-133a-2, mmu-mir-133b, mmu-mir-181b-2, mmu-mir-451a, mmu-mir-216b, mmu-mir-691, mmu-mir-181d, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, mmu-mir-129b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
However, ISH detection of other retina-specific miRs, including miR-213, miR-216, and miR-217, was unsuccessful in retina [26, 27].
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