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14 publications mentioning dre-mir-125a-1

Open access articles that are associated with the species Danio rerio and mention the gene name mir-125a-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 38
Although Lin28 and Bak1 have been proposed as the critical targets of miR-125a/b for regulating these stem cell compartments [8], [9], the hundreds of predicted targets for miR-125a/b suggest a more complex interplay between miR-125a/b and its targets in regulating proliferation and differentiation. [score:9]
miR-125a-AS was co -transfected with miR-125b-AS to achieve a complete silencing of the miR-125a/b family, because miR-125a, which shares the same seed sequence and the same predicted targets as miR-125b, is also highly expressed in human and mouse fibroblasts (Figure S1C, S1D). [score:5]
Overexpression of miR-125a/b causes an expansion of mammalian hematopoietic stem cells (HSCs) and aberrant differentiation, leading to myeloid leukemia [9], [10] and also lymphoid leukemia if miR-125b is overexpressed in fetal liver HSC-enriched cells [12]. [score:5]
Genes that were either significantly repressed by miR-125b or significantly derepressed by miR-125a/b-AS with fold-changes within the range of microRNA regulation (P<0.05, fold change > 1.3), were selected as candidate miR-125b targets (Figure 2B–2D). [score:4]
However, the molecular underpinnings of miR-125a/b's regulation of tissue stem cell homeostasis had remained unclear largely due to the complex nature of microRNA regulation of gene networks. [score:3]
In mice, out of 22 predicted targets in the p53 network, 11 genes were derepressed by miR-125a/b-AS in 3T3 cells and 12 genes were repressed by miR-125b in N2A cells (Figure 2C). [score:3]
Much like lin-4′s role of regulating the homeostasis of reiterative or self-renewing stem cells in C. elegans [6], recent studies have shown that miR-125a/b regulates mammalian neural stem cell commitment, as well as the mammalian hematopoietic stem cell (HSC) pool size [7]– [10]. [score:3]
Our GOF/LOF screen revealed that in humans, out of 29 predicted targets in the p53 network, 13 genes were derepressed by miR-125a/b-AS in hLF cells and 20 genes were repressed by miR-125b in SH-SY5Y cells (Figure 2B). [score:3]
1002242.g002 Figure 2(A) Loss-of-function (LOF) screens were performed in human primary lung fibroblasts (hLF) or mouse 3T3 fibroblasts by transfecting an antisense RNA against both miR-125a and miR-125b (miR-125a/b-AS), or by microinjecting morpholinos (MO) against pre- mir-125b hairpin precursors (all 3 isoforms) into zebrafish embryos. [score:1]
Several miRNAs are conserved in metazoan evolution, one prominent example being lin-4 whose vertebrate homologues comprise the miR-125a/b family [5]. [score:1]
In all panels, the levels of miR-125a and miR-125b were quantified by real-time PCR, and presented as log [2] (fold change) ± s. e. m. (n≥3) relative to the levelsof RNU6B loading control. [score:1]
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[+] score: 37
Evidences demonstrated that, in some cases, miR-125 could directly downregulate p53 and further influence the downstream protein p21 which is a CDK inhibitor [61, 62]. [score:7]
Based on TargetScan bioinformatic algorithm, zebrafish p53 was also identified as a potential target of miR-125 with a putative binding site on the 3′UTR, which is not verified in the current study but provides a new direction for the follow-up study. [score:6]
MiR-125 family is highly conserved throughout evolution, and it was demonstrated to regulate tumorigenesis and tumor development by targeting important genes including transcription factors like CBFB and TGF-β [52, 53], anti-apoptotic genes like BCL2, BCL2L12 and Mcl-1 [54], pro-apoptotic protein Bak1 [55], and tumor suppressing protein p53 [55, 56]. [score:6]
Recent studies have exhibited the dual function of miR-125 family as tumor suppressor and promotor, and the aberrant expression of miR-125 family is tightly related to tumorigenesis [43, 44]. [score:5]
Both miR-125a and miR-125b play excellent roles in the zebrafish brain development [67], meanwhile miR-125b also regulates the zebrafish eye development [67]. [score:4]
It was reported that miR-125 family has a dual function in suppression and promotion of cancer cells [44]. [score:3]
Interestingly, we identified a putative binding site of miR-125 on zebrafish cdc25a 3′UTR by TargetScan, which is absent on the CDC25A 3′UTR of both human and mouse. [score:3]
Recently, miR-125 has been confirmed to be hypoxia -induced in human cancer cells [7], also it was demonstrated to function in the transgenerational effect of hypoxia in medaka testis [48]. [score:1]
The miR-125 family, a highly conserved miRNA family throughout evolution, has been demonstrated to be implicated in a variety of physiological processes, including cell proliferation and apoptosis [39, 40], cell metastasis [41] and immune response [42]. [score:1]
Furthermore, miR-125a is demonstrated to be hypoxia -induced in human cancer [7]. [score:1]
[1 to 20 of 10 sentences]
[+] score: 32
As development proceeded, let-7 and miR-125a/b expression levels were increased, and expression levels of Lin28 and Lin41 were prominently downregulated in a reciprocal pattern. [score:9]
In the C. elegans heterochronic pathway, let-7 and lin-4/miR-125 miRNA play an essential regulatory role in the timing of stage-specific cell lineage development in nematodes, in part by directly regulating their target genes [5], [6], [13], [14]. [score:7]
Lin-28a and Lin-28b Regulate the Expression of Downstream Heterochronic Genes, as well as the miR-430 miRNA familyIn the C. elegans heterochronic pathway, miRNAs, including let-7 and lin-4/miR-125, play a critical role as downstream genes of lin28. [score:4]
On the other hand, let-7 and miR-125 are reportedly expressed in a reciprocal fashion to Lin28a and Lin41 during mouse development [36], [39] (Figure 6C). [score:4]
For example, let-7 and lin-4/miR-125 are highly conserved and expressed in various species, including Drosophila and humans [20], [34], [35]. [score:3]
Moreover, lin-41 and lin-28 are highly conserved in mammals and are regulated by let-7 and miR-125 like C. elegans [22], [36]. [score:2]
For example, in has been suggested that Lin28, let-7 and miR125 play important roles in cell fate determination in ES cells [24]. [score:1]
In the C. elegans heterochronic pathway, miRNAs, including let-7 and lin-4/miR-125, play a critical role as downstream genes of lin28. [score:1]
For example, lin-4/miR-125 miRNA promotes the transition between the first and second larval stages (L1 and L2, respectively) by binding to complementary sites in the 3′UTR of the upstream heterochronic genes lin-14 and lin-28 [3], [6], [15]– [17]. [score:1]
[1 to 20 of 9 sentences]
[+] score: 12
It is tempting to speculate that the miR-125 family—the mammalian homolog of the C. elegans heterochronic miRNA lin-4-is also targeted by Zcchc11 and Zcchc6 due to its known role in development, yet the mechanism of this targeting remains unknown. [score:6]
Interestingly, miR-125 family members are expressed from some of these same genomic clusters but do not contain the predicted targeting sequence. [score:5]
Still, they are highly uridylated in cultured HeLa cells and undergo a robust decrease in uridylation after loss of Zcchc11 and Zcchc6, and this is particularly true for miR-125a which was the most highly uridylated mature miRNA in our study. [score:1]
[1 to 20 of 3 sentences]
[+] score: 11
Of the miRNAs selected for comparison, two miRNAs (dre-miR-31 and dre-miR-430a) were up-regulated whereas two miRNAs (dre-miR-125a and dre-miR-126) were down-regulated based on the results of microarray analysis. [score:7]
In the present studies, expression changes in miR-430 and miR-125 families were quite significant. [score:3]
To validate the microarray data, we assayed expression levels of four miRNAs (dre-miR-125a, dre-miR-126, dre-miR-31, and dre-miR-430a) by qPCR and compared the results from the microarray and qPCR. [score:1]
[1 to 20 of 3 sentences]
[+] score: 10
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-204-1, dre-mir-181a-1, dre-mir-214, 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-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-25, dre-mir-26a-1, dre-mir-26a-2, dre-mir-26a-3, dre-mir-30d, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-100-1, dre-mir-100-2, dre-mir-125a-2, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-125c, dre-mir-126a, dre-mir-143, dre-mir-146a, dre-mir-462, dre-mir-202, dre-mir-204-2, 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-1388, dre-mir-222b, dre-mir-126b, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-204-3
The most enriched GO term was segment polarity determination (GO:0007367), which contained target mRNA for the miR-10 and miR-125 families, as well as miR-181a-5p miR-21-5p, miR-222a-3p, and miR-430b-3p. [score:3]
Sertoli cells with a Dicer -knockout mutation lacked several miRNAs, including miR-125a-3p, while having an overabundance of SOD-1, a protein linked to apoptotic cell death 43. [score:3]
miR-222a-3p was the only miRNA with no significant change in abundance over time, while miR-10a-5p, miR-10c-5p, miR-125a-5p, miR26a-5p, and miR-92b-3p showed no significant change in abundance from 3 to 12 wpf. [score:1]
Several miRNAs were consistently more abundant in testis than ovary, including miR-125a-5p, miR-125b-5p, miR-125c-5p, and miR-462-5p, whereas miR-22a-3p and miR-430b-3p were more abundant in the ovary (Fig. 6). [score:1]
Of the testis-enriched miRNAs, the let-7 family was well represented at 6 wpf (Fig. 6a), while the miR-125 family was abundant at 6, 9, and 24 wpf (Fig. 6a,b,d). [score:1]
In addition, miR-10b-5p, miR-125a-5p, miR-143–3p, miR-181a-5p, and miR-21–5p were among the most abundant miRNAs in at least six of nine gonadal stages (Fig. 4b). [score:1]
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[+] score: 6
Inhibition of three miRNAs, let-7, miR-125, and miR-9, caused similar defects in retinal development shown in Dicer1 conditional knock-out mice, further confirming that miRNAs are essential for early retinal development [23]. [score:6]
[1 to 20 of 1 sentences]
[+] score: 4
Other miRNAs from this paper: dre-mir-107a, dre-mir-125a-2, dre-mir-107b
Our results indicate that the level of miR107, but not miR125a, was up-regulated dramatically due to GRP94 depletion in ESCC (data not shown). [score:4]
[1 to 20 of 1 sentences]
[+] score: 3
In mouse, miR-125 is highly expressed in hematopoietic stem cells (HSCs) to expand HSC numbers in vivo [21]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
0053823.g002 Figure 2 The figure shows predicted binding alignment of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20*, miR-210*, miR-29a, miR-29b and miR457a with predicted zebrafish lncRNA. [score:1]
The miRanda software identified potential binding sites of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20a*, miR-210*, miR-2187, miR-29a, miR-29b and miR-457a in the predicted zebrafish 7sl lncRNA (Figure 2). [score:1]
The figure shows predicted binding alignment of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20*, miR-210*, miR-29a, miR-29b and miR457a with predicted zebrafish lncRNA. [score:1]
[1 to 20 of 3 sentences]
[+] score: 2
Northern blot of miR-125 mature sequence expression obtained upon biogenesis assay of miR-125-a1, -a2, -b1, -b2 and -b3 mutants and wild type pri-miRNA genes (bottom). [score:2]
[1 to 20 of 1 sentences]
[+] score: 2
As was similarly noted for lin-41 in C. elegans, Mlin41 also appears to be regulated by the let-7 and mir-125 miRNAs. [score:2]
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[+] score: 1
Furthermore, eight of the E2-repressed miRNAs also contained the AGGGU motif in their terminal loop (let-7 family members, miR-26a and miR-125a), whereas this motif does not exist in any of the control miRNA terminal loop sequences (Table S2). [score:1]
[1 to 20 of 1 sentences]
[+] score: 1
Single nucleotide polymorphism associated with mature miR-125a alters the processing of pri-miRNA. [score:1]
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