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9 publications mentioning rno-mir-363

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-363. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 26
Comparable to miR-298, hypoxia and DOR activation also downregulated miR-370 and miR-363* expression after 1-day treatment. [score:6]
Prolonged (10 days) UFP-512 treatment alone downregulated miR-363* expression by 50% when compared to controls, but no other statistically significant difference was noted. [score:5]
UFP-512 exposure increased miR-363* expression within 24 hours. [score:3]
The cortical miR-363* expression did not change in response to 1, 5 or 10 days of oxygen deprivation. [score:3]
DOR activation significantly reduced miR-363* expression by over 70% after 5 days of hypoxia (Figure 6a). [score:3]
Note that combination of hypoxia and UFP-512 treatment significantly altered the expression levels of miR-363*, -370, -21 and miR-31 in the cortex following 10-day treatment. [score:3]
Relative miRNA expression levels of miR-363*, -370, -21 and miR-31 in the rat cortex following 1, 5 or 10 days of hypoxia with or without UFP-512 treatment. [score:3]
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[+] score: 21
The mRNA encoding the cyclin dependent kinase inhibitor 1c (Cdkn1c) was up-regulated 3-fold in E13 ENPs and is predicted to be targeted by three miRNAs that were down-regulated: miR-92, miR-222, and miR-363-3p. [score:11]
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
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[+] score: 16
Age-specific changes in miRNA expression were found for miR-296*, miR-196a (Figure  5H-I), miR-181a, miR-214, miR-363, and miR-18a (Figure  6D-G) which showed high expression at 2 weeks of age in both sexes, followed by low and decreasing expression at all subsequent ages. [score:7]
MiR-363 is a member of the miR-92a family and its 2-week expression is consistent with its role in the formation of vascular endothelial cells during mammalian organ development [42]. [score:4]
MiRNAs associated with young age expression showed the highest enrichment for pathways involved in renal inflammation/nephritis (miR-130b, miR-363, miR-296*) and cancer (miR-214, miR-130b, miR-18a, miR-181a, miR-363, miR-196a). [score:3]
IPA infrequently associated a rat miRNA with a miRNA family gene name represented by a human miRNA of different name (e. g., rno-miR-363 is affiliated with miR-92a in gene list mapping); thus, miR-363 is associated with miR-92a in the Ingenuity knowledgebase for purposes of functional analysis. [score:1]
More than 15 cancer-related pathways ranked among the top findings for the young age group and included common miRNAs: miR-363, miR-181a, miR-130b, and miR-18a (Figures  5 and 6). [score:1]
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[+] score: 15
DOR treatment alone did not significantly alter basal miR-363* levels in the normoxic kidney, but prevented hypoxia -induced miR-363* down-regulation (Figure 3a). [score:4]
Relative miRNA expression levels of miR-363*, miR-let-7f, and miR-370 in the kidney following 10 days of hypoxia as determined by quantitative RT-PCR. [score:3]
Chronic hypoxia for 10 days depressed miR-363* expression greater than 50%. [score:3]
For example, chronic hypoxia largely reduced expression of miR-363*. [score:3]
DOR activation prevents the hypoxic reduction of miR-363*, suggesting that DOR signaling may regulate miR-363*, thus reducing hypoxic/ischemic injury. [score:2]
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[+] score: 10
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
Most had peak increases relative to controls at the 8-hour (n = 21) or 24-hour (n = 21) post-treatment time points, with one miRNA (miR-23a) having peak increase at the 1-hour time point, one miRNA (miR-363) having a peak increase at the 4-hour time point, and 2 miRNAs (miR-21, miR-99) with peak increases at the 48 hour time point. [score:1]
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[+] score: 7
On the 14th day after injury, 25 miRNAs, including miR-31a-3p, miR-17-5p, miR-146b-5p, miR-154-3p, and miR-363-3p, were upregulated (Figure  2C), and 18 miRNAs were downregulated, including miR-433-3p and miR-496-3p (Figure  2D). [score:7]
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[+] score: 3
Our previous study demonstrated that several miRNAs were differentially expressed in blood samples of DN patients by miRNA array and real-time PCR, including let-7a, let-7d, let-7f, miR-363, and miR-4429 (data not shown). [score:3]
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[+] score: 2
At 24 hours, five miRNAs (rno-miR-214, rno-miR-99a, rno-miR-363*, rno-miR-100 and rno-miR-340–5p) and at 48 hrs 6 miRNAs (rno-miR-34b, rno-miR-500, rno-miR-24-1*, rno-miR-29b, rno-miR-199a-3p, rno-let-7a) showed the most prominent dysregulation (P < 0.001) (Fig.   7B). [score:2]
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[+] score: 1
This cluster has two paralogs, miR-106a~363 (miR-106a, miR-18b, miR-19b-2, miR-20b, miR-92a-2 and miR-363, located on the X chromosome) and miR-106b~25 (miR-106b, miR-93, and miR-25, located on human chromosome 7), which are located on different chromosomes but contain individual miRNAs that are highly similar to those encoded by the miR-17~92 cluster [36, 37]. [score:1]
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