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13 publications mentioning rno-mir-99b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-99b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 37
UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
0180490.g006 Fig 6 UNX combined with HSD intake upregulates AT1R, LTCCs leading to increased cardiovascular reactivity and decreased BRS; upregulates miR-25, miR-155 and miR-451 and downregulates miR-99b affecting SERCA2, AKT and AMPK leading to impaired excitation-coupling cycle, fibrosis and hypertrophy culminating in cardiac dysfunction. [score:10]
miR-99, which regulates the expression of AKT [30] along with miR-155 [31], got downregulated in HSD, UNX and UNX+HSD (Fig 5E). [score:7]
The reason for downregulation of miR-99b in UNX is not known. [score:4]
In the experimental mo del of wound healing, miR-99b was shown to affect the expression of AKT [30]. [score:3]
D), E) Relative levels of miR-25, miR-155, miR-451 and miR-99b in heart normalized with sn-RNU5G; F) Relative levels of miR-25, miR-451 and miR-99b in plasma normalized with miR-30e. [score:1]
Micro RNAs quantified were hsa-miR-25-3p (Cat# 204361), mmu-miR-155-5p (Cat# 205930), hsa-miR-99b-3p (Cat# 204064) and mmu-miR-451(Cat# 204734) and normalized with RNU5G (a small nuclear RNA) in heart and hsa-miR-30e-5p (Cat# 204714) in plasma. [score:1]
Level of miR-99b coincided with the level of p-AKT1 in heart of HSD, UNX+HSD rats. [score:1]
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2
[+] score: 35
As a result, five up-regulated miRNAs (miR-874-3P, miR-20a-5p, miR-345-3p, miR-365-5p and miR-764-3p) and one down-regulated miRNA (miR-99b-3p) were screened out for subsequent qRT-PCR confirmation. [score:7]
For instance, the expression of miR-20a was found to be up-regulated whilst the miR-99b level was significant reduced in both of these two studies. [score:6]
0078375.g002 Figure 2The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
After analyzing the initial results of deep sequencing, six deferentially expressed miRNA (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) were screened out based on the criteria mentioned in, and qRT-PCR was performed to confirm their alterations after SE. [score:3]
More importantly, we found that the expression of miR-365-5p and miR-99b-3p were significantly correlated with neuronal apoptosis after SE. [score:3]
As shown in Figure 2, the expression of miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p was significantly increased after SE (P<0.05), whereas the levels of miR-99b-3p was markedly decreased (P<0.05). [score:3]
Furthermore, the expression of miR-99b-3p started to decrease at 24 hours after SE (P<0.05), reached its bottom at 1 week (P<0.05) and returned to basal levels at 3 weeks after SE (Figure 3F). [score:3]
The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. [score:3]
Correlations between levels of miR-365-5p and miR-99b-3p and apoptosis index. [score:1]
Taken together, these data confirmed that miR-345-3p and miR-99b-3p was involved in the pathogenesis of SE by modulating neuronal apoptosis. [score:1]
More importantly, miR-365-5p and miR-99b-3p have been revealed to be significantly correlated with neuronal apoptosis. [score:1]
We also observed a negative correlation between miR-99b-3p and apoptosis index (Figure7C and 7D, CA1: R = 0.850, P = 0.032; CA3: R = 0.930, P = 0.007). [score:1]
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3
[+] score: 28
To be specifically mentioned (fold change >2.5), miR-208, miR-19b, miR-133b and miR-30e were significantly upregulated and miR-99b, miR-100, miR-191a, miR-22 andmiR-181a-1 were significantly downregulated. [score:7]
The summary of the miRNAs significantly differentially expressed are provided in Table 1. Our study revealed the significant downregulation of miR-99 family (Fig. 2A,B) that comprises of three miRNAs such as miR-99a, miR-99b and miR-100, which are present in 11, 1, 8 chromosomes respectively. [score:6]
miR-99b IGF1R, Akt, mTOR The expression of miR-99b was highly downregulated during physiological hypertrophy. [score:6]
miR-99b, miR-100, miR-191a, miR-22 and miR-181a were significantly downregulated during hypertrophy (Fig. 2B). [score:4]
This miR-99 family mainly targets Akt/mTOR/IGF1 axis that leads to increased apoptosis and decreased protein synthesis during cancer. [score:3]
This is the first report to showcase the significant role of miR-99 family during cardiac hypertrophy. [score:1]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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4
[+] score: 25
In acute cell culture mo dels, overexpressing members of the miR-99/100 family inhibits gene expression and protein translation of mTORC1 signaling proteins, downregulating the activity of the pathway and ultimately cellular proliferation (Jin et al., 2013; Wei et al., 2013; Jia et al., 2014). [score:12]
In human muscle, diminished miR-99 and miR-100 expression predict the anabolic response to a resistance exercise bout, with reduced expression of these miR upregulating mTORC1 signaling (Zacharewicz et al., 2014). [score:8]
miR-99b -targeted mTOR induction contributes to irradiation resistance in pancreatic cancer. [score:3]
MicroRNA-99 family targets AKT/mTOR signaling pathway in dermal wound healing. [score:2]
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5
[+] score: 22
Calcineurin Aα (PPP3CA) is a predicted target of miR-21 and miR-99b (TargetScan 6.2) and is expressed more in epicardium than endocardium [113]. [score:7]
TargetScan 6.2 predicts 307 conserved targets for hsa-miR-21, 56 for hsa-miR-99b and 154 for hsa-miR-486-5p. [score:5]
We have found that most miRNAs are not expressed in a gradient across the ventricular wall, with the exceptions of miR-10b, miR-21, miR-99b and miR-486. [score:3]
05) transmural expression gradients for miR-10b, miR-21, miR-99b and miR-486 (Fig. 10). [score:3]
Enrichment of miR-99b was found in cardiac valves [116], although there is no available evidence for a role of miR-99b in valve disease. [score:3]
Thus a role for miR-21 and/or miR-99b in influencing transmural physiology is an intriguing possibility but requires further study. [score:1]
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6
[+] score: 4
The extent of downregulation can be categorized into three groups: one retaining less than 5% of the basal miRNA level in naïve animal (miR-10a, -98); one maintaining 5~15% (miR-99, -124a, -183) and one showing more than 25% left (miR-29a, -134). [score:4]
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7
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
A few pri-miRNAs exhibit conservation along the entire length of the pri-miRNA (for example mir-497~195, mir-99b~let-7c~mir-125a, mir-124-2, mir-130a and mmu-mir-568) (Figure 10). [score:1]
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8
[+] score: 3
Twelve miRNAs (miR-135a, miR-190, miR-22, miR-347, miR-376*, miR-380*, miR-382, miR-383, miR-702-3p, miR-708, miR-873, and miR-99b*) were regulated only in CCE rats (p < 0.05 vs. [score:2]
Other miRNAs, such as miR-181c, miR-191, miR-22, miR-99b*, and miR-369-5p, are also differentially modulated in rat hippocampus during post-status epilepsy [21, 22]. [score:1]
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9
[+] score: 3
We found that the expression patterns of most of these miRNAs revealed by qPCR were consistent with deep-sequencing results (Figure 2) with the exception of only four miRNAs (rno-miR-296, rno-miR-93, rno-miR-99b and rno-miR-130a), which exhibited minor discrepancy between qPCR and deep-sequencing results at P0. [score:3]
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10
[+] score: 2
MicroRNA-100 (miR-100), a member of miR-99 family (including miR-99a, miR-99b, miR-100), is a key apoptotic regulator in various cell types [24, 25]. [score:2]
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11
[+] score: 2
Conserved microRNA signatures were identified in valves (miR-let-7c, miR-125b, miR-127, miR-199a-3p, miR-204, miR-320, miR-99b, miR-328 and miR-744) and in ventricular-specific regions of the myocardium (miR-1, miR-133b, miR-133a, miR-208b, miR-30e, miR-499-5p, miR-30e*) of Wistar rat, Beagle dog and cynomolgus monkey. [score:1]
An assessment of the degree of conservation for structure-specific distribution of microRNAs in Wistar rat, Beagle dog and cynomolgus monkey (see for relative enrichment analysis), revealed high enrichment of nine microRNAs cardiac valves (miR-let7c, mIR-125b, miR-127, mir-199a-3p, miR204, miR-320, miR-99b, miR-328 and miR-744) (Figure 3A) and seven microRNAs in the myocardium (miR-1, mir-133a, miR-133b, miR-208b, miR-30e, miR-499-5p, miR-30e*) (Figure 3A). [score:1]
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12
[+] score: 1
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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13
[+] score: 1
The authors also demonstrated that resilient rats differed from vulnerable rats in the set of multiple blood-circulating miRNAs, namely, reduction in miR-139-5p, miR-28-3p, miR-326-3p, and miR-99b-5p in resilient animals and reduction in miR-24-2-5p, miR-27a-3p, miR-30e-5p, miR-3590-3p, miR-362-3p and miR-532-5p levels in vulnerable animals. [score:1]
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