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6 publications mentioning gga-mir-96

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-96. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 75
A longitudinal miRNA gradient may be significant for regulating gene expression, as microarray expression data revealed that predicted targets for both miR-182 and miR-96 were enriched in the basal (proximal) BP at P0, where the miRNA levels are lower [13]. [score:8]
At this stage, the control ear shows weak expression of miR-96 in vestibular organs and the vestibular ganglion (A) but no expression in the BP (D). [score:5]
Morpholino -mediated knockdown of the miR-183 family members decreased the number of HCs and otic neurons at 48 hours post fertilization (hpf), while overexpression of miR-96 or miR-182 resulted in ectopic and expanded sensory patches at 26 hpf [26]. [score:4]
The reductions obtained were 89% knockdown for the miR-96 reporter, 82% knockdown for the miR-182 reporter and 88% knockdown for the miR-183 reporter. [score:4]
At S28, expression of miR-96 is detected in the cristae (A, B), the utricular and saccular maculae (B), and the vestibular and cochleolagenar ganglia (B, C). [score:3]
At S32, miR-96 expression is robust in HCs of all three cristae (D, E, G) and the three maculae (H, J). [score:3]
These data suggest that HCs are particularly sensitive to the levels of wildtype miR-96, but do not rule out the possibility of a gain-of-function effect in which miR-96 [Dmdo] binds to inappropriate targets. [score:3]
In situ hybridization was used to detect the expression of mature miR-183, miR-96 and miR-182 on sections through the embryonic chicken inner ear at stages when nascent HCs are present in vestibular and auditory sensory organs (E5/S28 and E7/S31, respectively). [score:3]
In the zebrafish inner ear, overexpression of miR-96 or miR-182 induced ectopic sensory patches and extra HCs at 26 hpf [26]. [score:3]
The expression of miR-96 in the inner ear at S28 and S32. [score:3]
There is ectopic expression of miR-182 and miR-96 in the sensory and non-sensory epithelia and also in the vestibular and cochleolagenar ganglion neurons depicted in B, E, I and L. The signals detected by in situ hybridization are comparable to those shown by immunolabeling for GFP in nearby sections. [score:3]
The 3 members of the miR-183 family (miR-183, miR-96, miR-182) are processed from a single primary transcript [20, 21] and are expressed in sensory cells in mice and zebrafish [20, 22, 23]. [score:3]
The electroporated ear shows ectopic expression of miR-96 (arrows in B, E) in the inner ear epithelia that corresponds to GFP immunolabeling in nearby sections (arrows in C, F). [score:3]
Ectopic miR-96 expression can be observed two days after plasmid electroporation. [score:3]
Similar ectopic expression is observed for both miR-182 and miR-96 four days after plasmid electroporation. [score:3]
The latter is notable because mutations in the MIR96 gene underlie inherited hearing loss in both human (DFNA50) and the Diminuendo mouse mutant [18, 19]. [score:2]
Dmdo has been mapped to a point mutation in the seed region of miR-96. [score:2]
Here, hsa-miR-96/182/183, mmu-miR-96/182/183 and dre-miR-182 stand for hsa-miR-96/182/183-5p, mmu-miR-96/182/183-5p and dre-miR-182-5p, respectively. [score:1]
Luminescence only decreased when the miR-96 reporter was co -transfected with pGFP-183F, but not pGFP-9 (Fig 3D). [score:1]
This result is notable considering that miR-96 plays an important role in HC maturation and survival in the mouse, as revealed by the phenotypes observed in Dimineundo (Dmdo) mutant mice [18, 53, 54]. [score:1]
Alternate sections are processed for detection of miR-182 or miR-96 by in situ hybridization, or immunostained for GFP and HCS-1 (to detect HCs) as indicated on the panels. [score:1]
Our data from the chick do not support the idea that it is the absolute levels of wildtype miR-96 in nascent HCs that drives their separation into different phenotypes. [score:1]
Controls for reporter specificity were conducted using an unrelated miRNA, miR-9 housed in the pGFP backbone (pGFP-9), and the miR-96 luciferase reporter. [score:1]
The LNA probes used were dre/hsa-miR-183, hsa-miR-96 and dre-miR-182. [score:1]
Among the gene sets with miRNA recognition sites statistically over-represented at the high-frequency end were those predicted to bind miR-182 and miR-96. [score:1]
The miRNA reporters, composed of two complementary miRNA binding sites (to either miR-183, miR-96, or miR-182) housed downstream of the Renilla luciferase gene, were co -transfected into DF-1 cells with pGFP-183F or pGFP. [score:1]
Alternate sections are processed for in situ hybridization of miR-96 (A, B, D, E) or immunostained with an anti-GFP antibody and AlexFluor-488 secondary antibody to enhance the detection of GFP (C, F). [score:1]
A similar gradient was evident in adjacent sections probed for miR-183 (n = 3/4 ears from 2 embryos) or miR-96 (n = 2/5 ears from 3 embryos, S3 Fig bracket). [score:1]
Gallus gallus mature miR-183 (gga-miR-183) sequence was obtained from miRBase while the miR-182 and miR-96 sequences were obtained from published Gallus gallus short RNA sequencing reads [31]. [score:1]
S1 Fig miR-96 is conserved among the four species, while miR-182 and miR-183 show differences in the last few nucleotides at their 3’ ends. [score:1]
miR-96 is conserved among the four species, while miR-182 and miR-183 show differences in the last few nucleotides at their 3’ ends. [score:1]
The sequence of miR-96 is fully conserved between these species, while miR-182 and miR-183 differ by 1–3 nucleotides at their 3’ ends, but are otherwise identical. [score:1]
This difference in hybridization signal has also been reported in the mouse retina, as the level of miR-182 was highest and miR-96 was lowest [20]. [score:1]
We suspect that we are too close to the detection threshold to always see radial gradients of miR-96 and miR-183 in the BP, but they are probably present nonetheless. [score:1]
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2
[+] score: 13
Expression patterns of miR-96, miR-182 and miR-183 in the development inner ear. [score:4]
Conversely, over -expressing miR-96 and -182 promotes hair cell production. [score:3]
Further, miR-96 can regulate differentiation of cochlear hair cells (Kuhn et al., 2011). [score:2]
miR-96 regulates the progression of differentiation in mammalian cochlear inner and outer hair cells. [score:2]
Knockdown of miR-96, -182 and -183 causes a reduction in the numbers of inner ear hair cells. [score:2]
[1 to 20 of 5 sentences]
3
[+] score: 6
The mean fold change of CRL-4023 was set to 1. Table 1Summary of in-silico analysis ID Confidence Gene Pathway let-7c High (predicted) NUMBL Notch Signaling miR-103a-3p Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-1202 High (predicted) NUMBL Notch Signaling miR-125b-5p High (predicted) NUMBL Notch Signaling miR-1268a Moderate (predicted) NUMBL Notch Signaling miR-200a-3p High (predicted) NUMBL Notch Signaling miR-6088 Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-200b-3p High (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-3665 Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-4651 High (predicted) NUMBL Notch Signaling miR-96-5p High (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling To validate Numbl as a target gene for let-7c, firstly, the putative binding site of let-7c in the Numbl 3′-UTR was identified using the TargetScan database and the resulting sequence homology at base pairs 626–632 are shown (Figure 2A, Supplementary Data 1). [score:5]
The mean fold change of CRL-4023 was set to 1. Table 1Summary of in-silico analysis ID Confidence Gene Pathway let-7c High (predicted) NUMBL Notch Signaling miR-103a-3p Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-1202 High (predicted) NUMBL Notch Signaling miR-125b-5p High (predicted) NUMBL Notch Signaling miR-1268a Moderate (predicted) NUMBL Notch Signaling miR-200a-3p High (predicted) NUMBL Notch Signaling miR-6088 Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-200b-3p High (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-3665 Moderate (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling miR-4651 High (predicted) NUMBL Notch Signaling miR-96-5p High (predicted) NUMB Clathrin -mediated Endocytosis Signaling, Notch Signaling A. AsPC-1 cells were left untreated (CO) or were treated with quercetin (Q, 50 μM). [score:1]
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4
[+] score: 4
For example, miR-96 is down-regulated at HH25 by 1.81-fold in duck, by 1.84-fold in quail and by 7.35-fold in chicken NC cells. [score:4]
[1 to 20 of 1 sentences]
5
[+] score: 3
Contrarily to miRNA paralogs miR-96-5p and miR-1271-5p [11, 13], the previously described GPC3 -regulating miRNAs, miR-219-5p and miR-520c-3p [21, 22] were below the cut-off (Supplementary Table 1) and thus not selected in our screening. [score:2]
A siRNA against GPC3 and the miRNAs miR-96-5p and miR-219-5p were used as positive controls [11, 13, 22]. [score:1]
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6
[+] score: 2
Several miRNAs, including the miR-183 family, miR-96, miR-15, miR-99, miR-100, miR-125, and miR-133, all might contribute to hair cell development and maintenance [23– 26]. [score:2]
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