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17 publications mentioning dme-mir-133

Open access articles that are associated with the species Drosophila melanogaster and mention the gene name mir-133. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 35
Among 154 coexpressed miRNAs, five mature miRNAs (dme-miR-1008-5p, dme-miR-133-3p, dme-miR-137-3p, dme-miR-13b-3p, dme-miR-932-5p) were differentially expressed between PD and control groups (p<0.05) (Table 2 and S5 Table). [score:5]
As four of the dysregulated miRNAs in PD flies including dme-miR-133-3p, dme-miR-137-3p, dme-miR-13b-3p and dme-miR-932-5p were brain enriched, we predicted targets of them and then submit to DAVID for Gene Ontology analysis (Fig 6 and S7 Table). [score:4]
Among the dysregulated miRNAs, miR-13b, miR-133 and miR-137 were highly conserved from Drosophila to H. sapiens and their expression was validated by qRT-PCR. [score:4]
Our study using high throughput sequencing of miRNAs identified miR-13b, miR-133, miR-137, miR-932 and miR-1008 consistently upregulated in early stage PD flies. [score:4]
We found that five miRNAs (dme-miR-133-3p, dme-miR-137-3p, dme-miR-13b-3p, dme-miR-932-5p, dme-miR-1008-5p) were upregulated in PD flies. [score:4]
0137432.g005 Fig 5 qRT-PCR were performed to validate the expression of dme-miR-13b-3p, dme-miR-133-3p and dme-miR-137-3p in control and PD flies. [score:3]
qRT-PCR were performed to validate the expression of dme-miR-13b-3p, dme-miR-133-3p and dme-miR-137-3p in control and PD flies. [score:3]
Lgr3 (Relaxin receptor) and AR2 (Galanin receptor) were predicted to be targeted by miR133-3p and miR-13b-3p respectively. [score:3]
Using high throughput small RNA sequenceing technology, we measured miRNA expression profiles of early stage PD flies and identified five dysregulated mature miRNAs (miR-13b, dme-miR-133, dme-miR-137, miR-932 and miR-1008). [score:2]
Among them, miR-13b, miR-133, miR-137 are brain enriched and highly conserved from Drosophila to Homo sapiens. [score:1]
Among them, dme-miR-133-3p, dme-miR-137-3p and dme-miR-13b-3p (the mature sequence both for dme-mir-13b-1 and dme-mir-13b-2) were highly conserved from flies to humans and enriched in nervous system. [score:1]
MiR-133a and miR-133b are human orthologs of dme-miR-133 and enriched in human brain. [score:1]
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2
[+] score: 25
Targeted deletions of miR-1 or miR-133 in mice generally result in impaired cardiac development and function (6 – 11). [score:4]
Although miR-1 and miR-133 cooperate to repress smooth muscle gene expression in the heart (6, 7, 10, 11), miR-1 promotes differentiation of striated muscle progenitors, whereas miR-133 maintains the undifferentiated state in vitro (5, 12, 13). [score:3]
To our knowledge, a selective mature miRNA-protein interaction that limits miRNA activity, independent of miRNA biogenesis, has not been reported and suggests that the differential activity of mature miRNAs, including bicistronically encoded miRNAs, such as miR-1 and miR-133, can be regulated by selective interaction with RNA -binding proteins. [score:2]
Because the miR-1 family promotes differentiation and the miR-133 family keeps muscle in a less mature, more proliferative state (5, 12, 13), the TDP-43- miR-1 family interaction may be important to control the balance of these co-transcribed miRNA families to promote development and maintain adult muscle homeostasis. [score:2]
Given the extended half-life of miRNAs and the observations from deep-sequencing studies that the miR-1 family accounts for up to half of accumulated miRNAs in cardiac and skeletal muscles (20, 21), directly controlling the activity of these critical myogenic regulators and their differential activity as compared with miR-133 may be important to maintain muscle homeostasis. [score:2]
The miR-1 and miR-133 family loci are under transcriptional control of key myogenic proteins including myogenin, MyoD, serum response factor (SRF), myocardin (MYOCD) (3, 4, 16), and myocyte-enhancing factor 2 (MEF-2) (17). [score:1]
FIGURE 1. TDP-43 interacts with the miR-1/miR-206 family, but not miR-133. [score:1]
A, sequence alignment of the miR-1/miR-206 family or the miR-133 family. [score:1]
We concluded that a protein or complex of proteins in C [2]C [12] cells preferentially interacts with the mature form of the miR-1/miR-206 family, but not miR-133, in vitro. [score:1]
We found a prominent band representing an miRNA-protein complex in C [2]C [12] lysates incubated with labeled miR-1 that was effectively lost with the addition of excess unlabeled miR-1 or miR-206, but not with unlabeled miR-133 (Fig. 1 B). [score:1]
This is consistent with the observation that miR-1 and miR-206 levels greatly exceed those of miR-133 in mature muscle (20, 21). [score:1]
To identify proteins that physically interact with and might regulate activity of the miR-1/miR-206 family, but not the miR-133 family (Fig. 1 A), we performed RNA electrophoretic mobility shift assays (EMSAs) seeking proteins that uniquely bind and alter the migration of these miRNAs. [score:1]
Here, we report that TDP-43, an RNA -binding protein that aggregates in individuals afflicted with ALS, physically associates with the mature form of the miR-1/miR-206 family of miRNAs in muscle cells, but not with the co-transcribed miR-133. [score:1]
The same band was observed when fluorescently labeled miR-206 was incubated with C [2]C [12] lysates and could be competed with either miR-1 family member, but not with miR-133 (Fig. 1 B). [score:1]
The miR-1 family, composed of miR-1 and miR-206, whose mature sequences are nearly identical, and the miR-133 family (1, 2) are highly conserved and are enriched in cardiac and skeletal muscle in species as distantly related as flies and humans (3 – 5) (see Fig. 1 A). [score:1]
TDP-43 decreased activity of mature miR-1 and miR-206, but not the co-transcribed miR-133 family, by preventing the bound miRNAs from associating with the RISC. [score:1]
In mammals, up to three genomic loci encode bicistronic transcripts to produce miR-133 and either miR-1 or miR-206. [score:1]
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3
[+] score: 17
Given the requisite role of miR-1 and miR-133 in cell survival and development, it is convincing to believe that the redundant transcription complexes directing miR-1 and miR-133a expression are elegantly developed to ensure cells to survive under evolutionary pressure. [score:5]
MiR-1 and miR-133 are muscle-enriched microRNAs, and they have been demonstrated as critical factors involved in both cardiac and skeletal muscle development and diseases [20- 25]. [score:4]
Given the importance of miR-1 and miR-133 in various cardiomyopathy developments, such as cardiac hypertrophy, understanding the precise control of SRF -mediated microRNA gene regulation in the heart will provide an additional perspective for the treatment of SRF dysfunction -mediated cardiomyopathy. [score:3]
Given that individual microRNAs regulate potentially dozens of genes, functions of miR-1 and miR-133 in cardiac muscle and skeletal muscle can be quite distinct [23, 26, 27]. [score:2]
Both miR-1 and miR-133 also participate in cardiomyopathy development including cardiac hypertrophy [25, 28], cardiac fibrosis [29, 30], and arrhythmia [30, 31]. [score:2]
For skeletal muscle, miR-1 facilitates myogenesis, and miR-133 promotes myoblast proliferation [20]. [score:1]
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4
[+] score: 15
It is impossible to determine from this analysis whether microRNAs have acquired more targets in one clade or lost targets in the other, but it is striking that both human homologs of the fly microRNAs miR-184 and miR-210 are expressed at low abundance across many human tissues, while the homologs of miR-10, miR-133, miR-125, let-7, and miR-285 are expressed overall at much higher levels [19]. [score:9]
We stress that the human homologs of miR-10 and miR-133 have average or below average numbers of predicted targets in human. [score:3]
However, certain microRNAs appear to have a significantly higher number of target genes in either humans (miR-10, miR-133, miR-125, let-7, and miR-285) or flies (miR-184 and miR-210). [score:3]
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5
[+] score: 5
Bmo-miR-133 may regulate two B. mori orthologs of Mus musculus miRNA targeted genes, SRF and Ptbp2 because of the perfect binding between miRNAs and the complementary sites. [score:4]
miRNAs having the most orthologs are mir-133 and mir-9, which are found in 25 and 23 animal species, including D. melanogaster and C. elegans. [score:1]
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6
[+] score: 5
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-27a, hsa-mir-29a, hsa-mir-101-1, dme-mir-1, dme-mir-2a-1, dme-mir-2a-2, dme-mir-2b-1, dme-mir-2b-2, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-101a, mmu-mir-124-3, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-137, mmu-mir-140, mmu-mir-142a, mmu-mir-155, mmu-mir-10b, mmu-mir-183, mmu-mir-193a, mmu-mir-203, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-183, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-222, hsa-mir-223, dme-mir-34, dme-mir-124, dme-mir-79, dme-mir-210, dme-mir-87, mmu-mir-295, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, dme-let-7, dme-mir-307a, dme-mir-2c, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-193a, 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-29a, mmu-mir-27a, mmu-mir-34a, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-210, mmu-mir-223, mmu-mir-222, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-411, hsa-mir-193b, hsa-mir-411, mmu-mir-193b, hsa-mir-944, dme-mir-193, dme-mir-137, dme-mir-994, mmu-mir-1b, mmu-mir-101c, hsa-mir-203b, mmu-mir-133c, mmu-let-7j, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, mmu-mir-124b
Conserved pre-miRNAs with small variance of 5′-isomiR arm abundances among the four species (e. g. let-7 in Table 3) have lower folding energies (box to the right) than those with large variance (e. g. miR-133 in Table 3). [score:1]
We observed that miRNA orthologues (miR-10, miR-133, miR-137 and miR-79 in Table 3) swapped major miRNAs and 5′-isomiRs and had largely different 5′-isomiR arm abundances across human, mouse, fruitfly and worm. [score:1]
Such seed shift, as previously reported (50), was also identified in miR-133-3p and miR-137-3p across fruitfly and human/mouse (Table 3), and found in miR-79-3p between fruitfly and worm. [score:1]
For example, the major fruitfly dme-miR-133 with the seed ‘UGGUCCC’ is located 2-nt away from the upstream bulge (few 5′-isomiRs), but in human, the 5′-isomiR with the same seed ‘UGGUCCC’ is 3-nt away from the upstream bulge in pre-miR-133a-1/2 hairpins (Supplementary Figure S3B), thus plausibly accounting for a higher 5′ end heterogeneity of miR-133a-1/2 in human. [score:1]
Two conserved miRNA families with multiple members, i. e. miR-133 and miR-10, had individual members with large differential 5′-isomiR arm abundances. [score:1]
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7
[+] score: 4
We note that mir-1 and mir-133 are co-located in physical proximity in organisms as diverse as honey bees, frogs, mice and men, and are well-documented regulators of myogenesis in other organisms [31]. [score:2]
Ame-mir-1 and ame-mir-133 may exhibit similar functions in honey bees. [score:1]
They include ame-mir-1, which is near ame-mir-133. [score:1]
[1 to 20 of 3 sentences]
8
[+] score: 3
Other miRNAs from this paper: dme-mir-2a-1, dme-mir-2a-2, dme-mir-2b-1, dme-mir-2b-2, dme-mir-9a, dme-mir-10, dme-mir-12, dme-mir-13a, dme-mir-13b-1, dme-mir-13b-2, dme-mir-276a, dme-mir-276b, dme-mir-210, dme-mir-31b, dme-mir-9c, dme-mir-306, dme-mir-9b, dme-mir-31a, dme-mir-309, dme-mir-316, dme-mir-317, dme-mir-2c, ame-mir-12, ame-mir-133, ame-mir-210, ame-mir-276, ame-mir-2-1, ame-mir-2-2, ame-mir-317, ame-mir-9a, ame-mir-9b, bmo-mir-9a, bmo-mir-10, bmo-mir-276, bmo-mir-31, bmo-mir-71, ame-mir-10, ame-mir-137, ame-mir-13a, ame-mir-2-3, ame-mir-29b, ame-mir-31a, ame-mir-375, ame-mir-71, ame-mir-932, dme-mir-193, dme-mir-375, dme-mir-932, dme-mir-970, dme-mir-971, dme-mir-989, dme-mir-137, dme-mir-1006, dme-mir-1007, bmo-mir-2a-1, bmo-mir-2a-2, bmo-mir-2b, bmo-mir-13a, bmo-mir-13b, bmo-mir-133, bmo-mir-210, bmo-mir-317, tca-mir-2-3, tca-mir-2-1, tca-mir-2-2, tca-mir-10, tca-mir-12, tca-mir-13a, tca-mir-13b, tca-mir-31, tca-mir-71, tca-mir-133, tca-mir-137, tca-mir-210, tca-mir-276, tca-mir-317, tca-mir-932, tca-mir-9b, bmo-mir-12, bmo-mir-137, bmo-mir-932, bmo-mir-9b, tca-mir-9a, tca-mir-970, ame-mir-13b, ame-mir-1006, ame-mir-316, bmo-mir-970, lmi-mir-276, lmi-mir-210, lmi-mir-10, lmi-mir-9a, bmo-mir-9c, bmo-mir-306a, bmo-mir-989a, bmo-mir-316, bmo-mir-1175, bmo-mir-9d, bmo-mir-750, bmo-mir-375, bmo-mir-306b, api-mir-137, api-mir-10, api-mir-276, api-mir-13a, api-mir-210, api-mir-29, api-mir-2a, api-mir-2b, api-mir-2c, api-mir-316, api-mir-317, api-mir-71, api-mir-971, api-mir-9a, api-mir-9b, api-mir-306, api-mir-3049, bmo-mir-989b, ame-mir-1175, ame-mir-193, ame-mir-989, ame-mir-3049, ame-mir-971, ame-mir-3770, ame-mir-9c, ame-mir-306, ame-mir-750, tca-mir-9c, tca-mir-316, tca-mir-9d, tca-mir-309a, tca-mir-3049, tca-mir-375, tca-mir-29, tca-mir-1175, tca-mir-750, tca-mir-989, tca-mir-309b, tca-mir-193, tca-mir-6012, tca-mir-9e, ame-mir-6037, ame-mir-6012, ame-mir-2b, tca-mir-309c, tca-mir-971b
In an attempt to find possible missing conserved miRNAs, we examined the A. pisum genome and the available expression data, finding the additional conserved miRNAs: Mir-133, Mir-193, two miRNAs of the MIR-210 family, Mir-750, Mir-375 and two miRNAs of the MIR-bg5 family. [score:3]
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9
[+] score: 3
A possibly noteworthy finding is that casein kinase 2 (CKII), which has a role in the Drosophila clock [45, 46], is predicted to be a target of miR-133, miR-210 and miR-276b. [score:3]
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10
[+] score: 2
These showed expression patterns similar to those found by sequencing (Figure 2b); however, a little inconsistency was shown in miR-133, miR-193 and miR-2c compared with the results of sequencing, possibly owing to the low sensitivity of digoxigenin (DIG)-labeled oligodeoxynucleotide probes or for other unknown reasons. [score:2]
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11
[+] score: 2
Number suffix indicates replicate number e. g. OV2: adult non-bloodfed ovary, replicate 2. Additional file 3: On the top, sequence and predicted RNA secondary structure of annotated aga-mir-133 precursor. [score:1]
On the bottom sequence and predicted RNA secondary structure of aga-mir-133 precursor identified in this study. [score:1]
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12
[+] score: 1
MiR-133, miR-219, miR-263a, miR-274, miR-281-2*, miR-282, miR-283 and miR-310 which are also collected in miRBase without cloning evidence, are also identified. [score:1]
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13
[+] score: 1
The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation. [score:1]
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14
[+] score: 1
Indeed, we were able to identify one copy of mir-133, two copies of mir-137, and three copies of mir-124 (supplementary file S4, online) in the genome of P. tepidariorum, further increasing the number of microRNAs that we identified. [score:1]
[1 to 20 of 1 sentences]
15
[+] score: 1
As with the let-7-C cluster in flies, members of polycistronic clusters, including the miR-17~92 and miR-1/miR-133 clusters, are differentially processed [64, 65]. [score:1]
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16
[+] score: 1
We have found two instances of microRNA clusters in animals whose individual microRNAs are apparently not clustered in Drosophila (mir-1/mir-133 and mir-276a/mir-276b; Table 2). [score:1]
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17
[+] score: 1
However, we did not identify those from adult testis such as miR-133, -223, or -155 [19]. [score:1]
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