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10 publications mentioning dre-mir-221

Open access articles that are associated with the species Danio rerio and mention the gene name mir-221. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 158
We also tested the effect of VEGF on the expression of miR-221/222 to examine whether they are downregulated in an angiogenesis-promoting environment. [score:6]
Overexpressing miR-221 in zebrafish caused deregulated blood vessel pattern but not the reduction of vessel density, which may partly due to the fact that miR-221 is required for vascular development by promoting tip cell migration and proliferation in zebrafish during vascular development [39]. [score:6]
Only miR-222, but not miR-221, inhibited ETS1 translation through both putative binding sites (Figure  5D). [score:5]
miR-221 and miR-222 each has unique targets and different mechanisms to repress the activities of diseased late EPCs (Figure  5F). [score:5]
We found ETS1 is among miR-222 -suppressed genes in late EPCs and possesses miR-221/-222 binding sites on its 3′UTR according to the TargetScan bioinformatics prediction (Figure  5B). [score:5]
Over -expression of either miR-221 or miR-222 in zebrafish embryos resulted in the deregulation of blood vessel pattern during development (Figure  4E, abnormal blood vessels indicated by arrows). [score:5]
Previous study indicated miR-221 may regulate the delicate stoichiometry of PIK3R1 subunit to maintain the correct subcellular localization and regulate downstream flt4 expression [39]. [score:5]
Overexpressing miR-221/222 reduced the in vitro cellular motility and microvasculature formation ability of late EPCs (Figure  4D), which partly explained why these 2 miRs were more abundant in disease EPCs and in mature ECs. [score:5]
Cloning and transient expression of miR-221/222 expression constructs were described [31]. [score:5]
Since neither miR-221 nor miR-222 targets CXCR4 directly according to bioinformatics prediction, how CXCR4 levels are regulated is still an open question. [score:5]
We demonstrated another candidate miR-221 target gene – PIK3R1, which is also important in regulating endothelial tip cell migration and proliferation in EPC [39]. [score:4]
To explore the underlying mechanisms, we aligned genes down-regulated by miR-221 and miR-222. [score:4]
Nevertheless, no miR-221- or miR-222 -binding site could be identified on CXCR4 mRNA (not shown), we searched for direct targets for either miRNAs. [score:4]
Endothelial progenitor cell smRNA-seq Circulating microRNA Coronary artery disease MicroRNA-221/222 Defect in angiogenesis or blood vessel repair is the major cause of complications of cardiovascular disorder (CVD) and many ischemia-related diseases, such as diabetes and stroke [1, 2]. [score:4]
Late EPC was found to possess the best angiogenic activities and less miR-221/222 expression. [score:3]
miR-221 and miR-222 also inhibit erythropoiesis and erythroleukemic cell growth via down-modulating cKit [50]. [score:3]
We observed defective vascular growth when miR-221 or miR-222, especially miR-222, was overexpressed in zebrafish. [score:3]
Overexpress miR-221 and miR-222 in zebrafish embryos. [score:3]
We found both miR-221 and miR-222 repressed in late EPCs the levels of chemokine (C-X-C motif) receptor 4 (CXCR4), the receptor for CXCL12 (Figure  4), partly explains why miR-221/222 inhibit late EPC motility (Figure  4C), and EPC levels were reduced in the peripheral blood of CAD patients. [score:3]
In contrast, PIK3R1 is the target of miR-221, but not miR-222 in late EPCs. [score:3]
When miR-221 and miR-222 were overexpressed in late EPCs, only miR-221, but not miR-222, repressed PIK3R1 (Figure  5E, lower panel). [score:3]
We also searched target(s) for miR-221 in CAD late EPCs. [score:3]
Examples like miR-221 and miR-222 are transcribed from the same miRNA cluster and are able to modulate the angiogenic properties of HUVECs by targeting c-Kit and endothelial nitric oxide synthase (eNOS) [17, 18]. [score:3]
Since miR-221 and miR-222 are known to target ETS2 and ETS1, respectively, in matured blood vessel endothelial cells [31], we tested whether ETS1 and ETS2 levels in late EPCs from CAD patients. [score:3]
Overexpression of miR-221 and miR-222 resulted in the reduction of genes involved in hypoxia response, metabolism, TGF-beta signalling, and cell motion. [score:3]
Since EPCs are capable of forming new blood vessels even in the absence of a pre-existing vessel network [6] and knockdown experiments showed that miR-221 is required for endothelial tip cell behaviors during vascular development [39], we examined the role of miR-221/222 in the formation of the blood vessels in vivo. [score:3]
The direct repression of ETS1 translation by miR-221 and miR-222 was examined by 3′UTR reporter assays. [score:3]
VEGF repressed the levels of matured miR-222 and pri-miR-221/222 in diseased late EPCs (Figure  4C). [score:3]
miR-221/222 inhibit EC [31] and EPC motility and microtubule formation. [score:3]
It has been reported that levels of miR-221 and miR-222 are higher in EPCs from patients with coronary artery disease (CAD) [19, 20], but the anti-angiogenic role of miR-221/222 and the downstream mechanism in late EPCs is unclear. [score:3]
We verified that late EPCs isolated from the peripheral blood of CAD patients expressed more miR-221/222, especially miR-221, than those from healthy controls (Figure  4A). [score:3]
It is known that miR-221 promotes tip cell behavior during vascular development through the repression of phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) [39]. [score:3]
Consistent with these observations, in late EPCs from CAD patients the expression levels of miR-221 and miR-222 are increased (Figure  4A) [20]. [score:3]
RT-qPCR show the levels of PIK3R1 in health and CAD late EPCs (upper), or in late EPCs overexpressed with miR-221. [score:3]
There are two miR-221/222 binding sites on 3′UTR of ETS1 (NM_005238) predicted by TargetScanHuman (http://www. [score:3]
Furthermore, levels of EPC miR-221/222 are significantly higher in patients with coronary artery disease (CAD) [19, 20]. [score:3]
In summary, our results demonstrate miR-221 and miR-222 repress the levels of PIK3R1 and ETS1, respectively to regulate angiogenic features in EPCs and ECs (Figure  5F) and suggest mechanisms of why late EPC levels and activities are reduced in CAD patients. [score:2]
Reporter assays showed that miR-222, but not miR-221, targets the angiogenic factor ETS1. [score:2]
Clinically, both miR-221-PIK3R1 and miR-222-ETS1 pairs are deregulated in late EPCs of CAD patients. [score:2]
Figure 5 miR-221 and miR-222 regulate PIK3R1 and ETS1, respectively, in late EPCs. [score:2]
However, miR-221 levels were not significantly affected by VEGF (Figure  4C), indicating a post-transcriptional event may also be involved in the regulation of miR-221 levels in CAD late EPCs. [score:2]
miR-221/222cluster miRNAs contribute to EPC motility and blood vessel formationConsistent with the less active nature of HUVEC (Figure  1C), two anti-angiogenic miRNAs, miR-221 and miR-222, were more abundant in matured ECs (Figure  1G). [score:1]
Twelve cell migration genes (AGT, CITED2, CXCR4, F2RL1, F3, HDAC6, IRS2, IGFBP3, PTEN, PIK3R1, PTPRM, & TGFBR3) were reduced in the presence of miR-221/222, consistent with the reduced cell motility phenotype in Figure  4D. [score:1]
miR-221/222 affect genes involved in hypoxia response, cell migration, energy supply and so on. [score:1]
miR-221 and miR-222 are two highly homologous miRNAs encoded in tandem from human chromosome Xp11.3 and are highly conserved in vertebrates. [score:1]
Figure 4 Decreased miR-221/222 levels in CAD patients and the contribution of miR-221/222 in late EPC functions. [score:1]
Obtained signatures made up of both novel and known microRNAs, in which anti-angiogenic microRNAs such as miR-221 and miR-222 are more abundant in matured ECs than in late EPCs. [score:1]
RT-qPCR using independent batches of cord blood EPCs verified that anti-angiogenic miRNAs such as miR-221-3p and miR-222-3p (was known as miR-221 and miR-222) [17, 18] were enriched in matured ECs (Figure  1G). [score:1]
Furthermore, circulating miR-221 and miR-222 levels in the plasma of CAD patients were found to be higher. [score:1]
Repression of CXCR4 levels by both miR-221 and miR-222 was confirmed by RT-qPCR (Additional file 6: Figure S1). [score:1]
Consistent with the less active nature of HUVEC (Figure  1C), two anti-angiogenic miRNAs, miR-221 and miR-222, were more abundant in matured ECs (Figure  1G). [score:1]
miR-222, but not miR-221, led to a significant reduction in blood vessel density in vivo (Figure  4F). [score:1]
miR-221/222cluster miRNAs contribute to EPC motility and blood vessel formation. [score:1]
More significantly, levels of circulating miR-221/222 in the plasma of CAD patients were also higher than those in healthy controls (Figure  4B, p < 0.0001). [score:1]
Embryos in the Tg(kdrl:EGFP) [s843] background were injected with 460 pg of negative control RNA (n = 100), 560 pg RNA of miR-221 (n = 106), or 560 pg RNA of miR-222 (n = 62). [score:1]
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2
[+] score: 21
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-mir-219-1, dre-mir-219-2, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-92b, dre-mir-96, dre-mir-100-1, dre-mir-100-2, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-135c-1, dre-mir-135c-2, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-153a, dre-mir-181c, dre-mir-200a, dre-mir-218a-1, dre-mir-218a-2, dre-mir-219-3, dre-mir-375-1, dre-mir-375-2, dre-mir-454a, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-181a-2, dre-mir-34b, dre-mir-34c, dre-mir-222b, dre-mir-138-2, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-128-3
For instance, miR-222 and miR-221 share largely similar expression in the adult hypothalamus (ATN, LH, Hd in Figure G of0 and Figure O of9) but only miR-222 is expressed in the ventral intermediate hypothalamus at the larval stage (Figure D of0 and Figure B of9; see also Table K in8 for other miRNAs belonging to a single cluster and7 tables for their expression). [score:7]
miR-221 expression in the zebrafish brain. [score:3]
Additional data file 19 is a figure showing miR-221 expression in the zebrafish brain. [score:3]
It is not obvious why there should be differences in miR-222 and miR-221 expression as they are present in the same cluster and one would predict that they are co-transcribed. [score:3]
Click here for file 9 miR-221 expression in the zebrafish brain. [score:3]
We compared the adult brain expression of miRNAs belonging to the same family, such as miR-181a and miR-181b, or cluster, such as miR-221 and miR-222, that differ in three and four nucleotides, respectively; LNA probes should, therefore, discriminate each of them. [score:2]
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3
[+] score: 9
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
Mdm2 is negatively regulated by several miRNAs including miR-192 (Pichiorri et al., 2010), miR-194 (Pichiorri et al., 2010), miR-215 (Pichiorri et al., 2010), miR-221 (Kim et al., 2010), and miR-17 (Li and Yang, 2012) in different cellular contexts; however, whether these or other miRNAs regulate Mdm2 expression during the CNS development must be determined. [score:6]
MicroRNA-221 regulates chondrogenic differentiation through promoting proteosomal degradation of slug by targeting Mdm2. [score:3]
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[+] score: 5
Overexpression of miR-181a, miR-181b, miR-221, miR-222 and miR-451 (10 µM) resulted in no observable phenotype in zebrafish embryos at 2 dpf. [score:3]
The miRNAs that did not produce any visible vascular phenotypes in our screen include miR-181a, miR-181b, miR-221, miR-222 and miR-451. [score:1]
Zebrafish embryos injected with miR-221, miR-222 and miR-451 display no observable phenotype (figure not shown). [score:1]
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5
[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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6
[+] score: 4
Other miRNAs from this paper: dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-210, dre-mir-214, dre-mir-219-1, dre-mir-219-2, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-21-1, dre-mir-21-2, dre-mir-25, dre-mir-30e-2, dre-mir-101a, dre-mir-103, dre-mir-107a, dre-mir-122, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-126a, dre-mir-129-2, dre-mir-129-1, dre-mir-130b, dre-mir-130c-1, dre-mir-130c-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-135c-1, dre-mir-135c-2, dre-mir-140, dre-mir-142a, dre-mir-142b, dre-mir-150, dre-mir-152, dre-mir-462, dre-mir-196a-2, dre-mir-196b, dre-mir-202, dre-mir-203b, dre-mir-219-3, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-mir-455-1, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-135b, dre-mir-135a, dre-mir-499, dre-mir-738, dre-mir-429b, dre-mir-1788, dre-mir-196c, dre-mir-107b, dre-mir-455-2, dre-mir-222b, dre-mir-126b, dre-mir-196d, dre-mir-129-3, dre-mir-129-4
The heart showed accumulation of dre-miR-101a, dre-miR-130b, dre-miR-130c, dre-miR-221 and dre-miR-499, while dre-miR-1 and dre-miR-133a expression was detected in both muscle and heart. [score:3]
For example, dre-miR-101a, dre-miR-130b, dre-miR-130c, dre-miR-221 and dre-miR-499 were highly enriched in the heart, in agreement with previous in situ and Northern blot studies [20]. [score:1]
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7
[+] score: 3
There is no evidence yet for such a mechanism in fish, but a recent computational study in human has predicted TFs, including Ap2a and Mitf, and small regulatory RNAs, such as mir-221, as shared upstream regulators of igsf11 and pmel in specific melanocyte lineages (Rambow et al., 2015). [score:3]
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8
[+] score: 2
So far, a number of non-coding regulators such as miR-451 (5, 6), miR-23a (7), miR-221/222 (8), miR-376a (9) and miR-223 (10) were reported to play positive or negative roles in controlling erythropoiesis. [score:2]
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9
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-221, hsa-mir-23b, hsa-mir-27b, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-200c, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-30e, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-10b-1, dre-mir-181b-1, dre-mir-181b-2, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-204-1, dre-mir-181a-1, dre-mir-222a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7e, dre-mir-7a-3, dre-mir-10b-2, dre-mir-20a, dre-mir-21-1, dre-mir-21-2, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-26b, dre-mir-27a, dre-mir-27b, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-30e-2, dre-mir-101b, dre-mir-103, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-148, dre-mir-181c, dre-mir-200a, dre-mir-200c, dre-mir-203b, dre-mir-204-2, dre-mir-338-1, dre-mir-338-2, dre-mir-454b, hsa-mir-181d, dre-mir-212, dre-mir-181a-2, hsa-mir-551a, hsa-mir-551b, dre-mir-31, dre-mir-722, dre-mir-724, dre-mir-725, dre-mir-735, dre-mir-740, hsa-mir-103b-1, hsa-mir-103b-2, dre-mir-2184, hsa-mir-203b, dre-mir-7146, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-204-3, dre-mir-24b, dre-mir-7133, dre-mir-128-3, dre-mir-7132, dre-mir-338-3
Although zebrafish miRNAs have been examined in numerous studies [25, 27, 41– 43], our analysis revealed novel paralogs of 18 miRNAs that do not currently have zebrafish records in miRBase (version 21), including miR-181a, miR-20a, miR-23b, miR-24, miR-29a, miR-103, miR-128, miR-148, miR-181b, miR-199, miR-204, miR-212, miR-221, miR-338, miR-724, miR-2184, let-7b and let-7e. [score:1]
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10
[+] score: 1
Other miRNAs from this paper: hsa-mir-23a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-205, hsa-mir-214, hsa-mir-221, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-184, hsa-mir-193a, hsa-mir-1-1, hsa-mir-29c, hsa-mir-133b, dre-mir-205, dre-mir-214, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-1-2, dre-mir-1-1, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-107a, dre-mir-122, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-184-1, dre-mir-193a-1, dre-mir-193a-2, dre-mir-202, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-202, hsa-mir-499a, dre-mir-184-2, dre-mir-499, dre-mir-724, dre-mir-725, dre-mir-107b, dre-mir-2189, hsa-mir-499b, dre-mir-29b3
Zhao J. J. Lin J. Yang H. Kong W. He L. Ma X. Coppola D. Cheng J. Q. MicroRNA-221/222 negatively regulates estrogen receptor alpha and is associated with tamoxifen resistance in breast cancerJ. [score:1]
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