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17 publications mentioning rno-mir-128-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-128-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 95
Among the three microRNAs (Shi et al., 2012; Xu et al., 2012, 2015) (miR-497-5p, miR-145-5p, miR-128-3p) previously reported to target p70s6k1 mRNA and inhibit its translation, only miR-128-3p was downregulated by TXL during I/R. [score:10]
By western blotting analysis, the miR-128-3p mimics downregulated expression and inhibited phosphorylation of p70s6k1 (Figure 7B). [score:8]
Further research will be needed to elucidate whether TXL decreases miR-128-3p levels by directly inhibiting the transcription of its gene or, instead, acts in an indirect manner, such as by facilitating expression of endogenous RNAs (e. g., lnc-LAMC2-1:1 Gong et al., 2016) that compete with miR-128-3p. [score:7]
Furthermore, p70s6k1 upregulation by TXL was attributable to downregulation of miR-128-3p in cardiomyocytes during I/R. [score:7]
Because of the decrease in p-p70s6k1/p70s6k1 levels in HCMs during H/R, TXL pretreatment no longer inhibited cell death in HCMs (Figure 7A), suggesting that upregulation of miR-128-3p abrogated the protective effects of TXL on HCMs. [score:6]
TXL downregulated miR-128-3p, a microrna targeting p70s6k1. [score:6]
However, in our study we found that, with inhibition of miR-128-3p, TXL enhanced p70s6k1 phosphorylation and, thus, activated the RISK pathway by facilitating p70s6k1 expression, rather than by activating Akt or Erk. [score:5]
Because TXL was reported to decrease expression of microRNAs and increase levels of their corresponding proteins under certain conditions (Wang J. Y. et al., 2014; Zhang et al., 2014, 2017), we used quantitative PCR to examine levels of several microRNAs (Shi et al., 2012; Xu et al., 2012, 2015) (miR-497-5p, miR-145-5p, and miR-128-3p) known to target the mRNA of p70s6k1 in HCMs (Figure 6B). [score:5]
In conclusion, we reveal for the first time that TXL can directly inhibit cardiomyocyte apoptosis and thus alleviate myocardial reperfusion injury through the miR-128-3p/p70s6k1 pathway. [score:4]
MicroRNA-128 inhibition attenuates myocardial ischemia/reperfusion injury -induced cardiomyocyte apoptosis by the targeted activation of peroxisome proliferator-activated receptor gamma. [score:4]
Figure 6TXL downregulated the level of miR-128-3p in cardiomycytes during H/R or I/R. [score:4]
To explore whether miR-128-3p was involved in the beneficial effects of TXL against H/R -induced apoptosis, mimics were utilized to upregulate levels of miR-128-3p in HCMs. [score:4]
MiR-128 inhibits tumor growth and angiogenesis by targeting p70S6K1. [score:4]
Moreover, miR-128-3p inhibition in cells enhanced their resistance to detrimental stimuli like chemotherapeutic agents and H/R (Zhu et al., 2011; Chen et al., 2016; Zeng et al., 2016). [score:3]
The inhibition of microRNA-128 on IGF-1-activating mTOR signaling involves in temozolomide -induced glioma cell apoptotic death. [score:3]
miR-128 and its target genes in tumorigenesis and metastasis. [score:3]
Another limitation is that we did not investigate how TXL downregulated miR-128-3p. [score:2]
H/R+TXL+miR-128 mimic; NC, negative control. [score:1]
MicroRNAs (miR-497-5p, miR-145-5p, and miR-128-3p) were reverse transcribed using miScript II RT Kit (Qiagen, Valencia, CA, USA) and then quantified by quantitative real-time RT-PCR using the miScript SYBR green PCR kit (Qiagen). [score:1]
When HCMs reached 70–80% confluence, small interfering RNA (siRNA) oligonucleotides against p70s6k1 (Santa Cruz Biotechnology), nonspecific control siRNA oligonucleotide (Santa Cruz Biotechnology), mimics of miR-128-3p (Thermo Fisher Scientific, Inc. [score:1]
Reduced miR-128 in breast tumor-initiating cells induces chemotherapeutic resistance via Bmi-1 and ABCC5. [score:1]
Brain microRNAs and insights into biological functions and therapeutic potential of brain enriched miRNA-128. [score:1]
The miR-497-5p, miR-145-5p, and miR-128-3p levels were determined with the 2 [(−ΔΔCT)] relative quantification method, using U6 as an internal control. [score:1]
Figure 7Transfection of miR-128-3p mimic abrogated the anti-apoptotic effects of TXL on HCMs during H/R. [score:1]
The protective effects of TXL on HCMs during H/R were largely abolished by transfection with miR-128-3p, indicating that miR-128-3p mediated the beneficial effects of TXL on HCMs during H/R. [score:1]
HCMs were transfected with miR-128-3p mimics, preconditioned with 400 μg/mL TXL and then subjected to H/R. [score:1]
A major limitation of our study was that we did not identify which ingredients in TXL, alone or in combination, were responsible for activation of the miR-128-3p/p70s6k1 pathway in cardiomyocytes during I/R. [score:1]
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[+] score: 32
Furthermore, five deregulated miRNAs (miR-128-3p and miR-34c-5p, both downregulated at P10; miR-19b-3p, miR-449a-5p and miR-30e-5p, these three being upregulated at P21) have E2F3 in common as a target gene. [score:10]
Among these miRNAs, three showed more than twofold differential expression (Fig 1): miR-128-3p and miR-34c-5p were significantly downregulated, and miR-434-3p was significantly upregulated. [score:9]
At P10, the differential expression of the three miRNAs was statistically confirmed, with miR128-3p and miR34c-5p downregulated and miR434-3p upregulated. [score:9]
Among the other miRNAs found deregulated in our study, miR-34c-5p, miR-128-3p miR-184, miR127-3p, miR-30e-5p, and miR-23b-5p were also previously described as “tumour suppressors”[22– 26], although many miRNA studies previously dealt with cancer or oncogenic proliferation states and the current analysis depended on previous reports. [score:4]
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[+] score: 30
The most regulated genes from MAPK pathway were: platelet derived growth factor receptor beta (PDGFRA), a target for miR-93-5p, 410-3p and 128-3p; MAP kinase-interacting serine/threonine kinase 2 (MKNK2), a target for miR-93-5p and 128-3p; Nuclear factor of activated T-cells 3 (NFATE3), a target for miR-128-3p and 103-3p; transforming growth factor beta receptor 1 (TGFBR1), a target for miR-128-3p and 142-3p; and nemo like kinase (NLK), a target for miR-3068-3p and 410-3p. [score:12]
The most regulated genes from the MAPK pathway were: platelet derived growth factor receptor beta (PDGFRA), a target for miR-93-5p, 410-3p, and 128-3p; MAP kinase-interacting serine/threonine kinase 2 (MKNK2), a target for miR-93-5p and 128-3p; Nuclear factor of activated T-cells 3 (NFATE3), a target for miR-128-3p and 103-3p; transforming growth factor beta receptor 1 (TGFBR1), a target for miR-128-3p and 142-3p; and nemo like kinase (NLK), a target for miR-3068-3p and 410-3p (Figure 3B). [score:12]
Eight miRNAs were downregulated after exercise: Rno-miR-128-3p (FDR = 0.0238), 103-3p (FDR = 0.0284), 148a-3p (FDR = 0.0342), 191a-5p (FDR = 0.0342), 93-5p (FDR = 0.0381), 25-3p (FDR = 0.0381), 142-5p (FDR = 0.0414), 3068-3p (FDR = 0.0454) (Figure 2B). [score:4]
In our results, we found out that rno-miR-128-3p, 103-3p, 148a-3p, 191a-5p, 93-5p, 25-3p, 142-5p, and 3068-3p decreased after exercise in rat serum EVs (Table 1). [score:1]
In humans, a miRNA profile from blood and plasma obtained from endurance and strength athletes, miR-128-3p showed correlation levels with the free testosterone (Pershing et al., 2015). [score:1]
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[+] score: 17
Overall, the expression patterns of miRNAs fell into four main categories: (1) Enriched in early embryonic stages, especially at E10 and E13 and decreased gradually during development (i. e. the rno-miR-181 family); (2) Enriched late postnatally, especially at P14 and P28, and tended to increase over time (i. e. rno-miR-29a and rno-miR-128); (3, 4) Peaked around neonatal stage (P0), either highest peak or lowest peak. [score:4]
One example is miR-128, which was reported to be specifically expressed in postnatal cortex [6]. [score:3]
However, our results showed that miR-128 was also expressed in embryonic cortex with much lower abundance, indicating that high throughput sequencing is much more sensitive than conventional methods. [score:3]
Click here for file Detail editing profile of miR-128 during cortical development. [score:2]
Detail editing profile of miR-128 during cortical development. [score:2]
A summary of the position, sequence, abundance (TPM) of each detected editing of miR-128 is shown. [score:1]
Taking rno-miR-128 as an example, highest frequency of “A” to “C” editing at position 3 and “G” to “T” editing at position 6 was observed at P14, whereas “G” to “T” editing at position 8 was highest at P3 (Figure S8). [score:1]
B. A summary of the sequence, length, and count of each isomiR of miR-128 in P14 cortical tissues. [score:1]
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[+] score: 13
The expression levels of these miRNA and mRNA are presented as ratios to the mean value in control tissue on day 3. The expression levels of miR-29a-3p and miR-128-3p in reflux esophagitis were significantly lower than those of the controls on day 3 (Figure 4A,B). [score:5]
Microarray analysis revealed an upregulation of miR-29a-3p, miR-128-3p, miR-223-3p and miR-3473 in reflux esophagitis (p < 0.05 compared to controls). [score:3]
The expression patterns of miR-29a-3p, miR-128-3p and miR-3473 were not dramatically changed during acute to chronic phases (Figure 4A,B,D). [score:3]
Analogously, the expression level of exosomal miR-128-3p in reflux esophagitis was significantly lower on day 3 compared with the control, but there was no significant difference on day 7 and 21 between control and reflux esophagitis (Figure 2B). [score:2]
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[+] score: 12
Moreover, it has been shown that the absence of miR-128 expression in miR-128-2−/− mice causes seizure -induced death, which is prevented by its overexpression [76]. [score:5]
Similar to our observation, prominent down-regulation of miR-128 has been recorded in the acute and chronic phase of Litio-PILO induced epileptogenesis [75]. [score:4]
In fact, the bioinformatics analysis of the validated targets of hsa-miR-128 showed a significantly over-representation of pathways such as P53, Insulin/IGF pathway-mitogen activated protein kinase kinase/MAP kinase cascade (Table 1), which are enhanced after SE insult. [score:3]
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[+] score: 12
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
We predict that several of the differentially regulated genes are miRNA targets and miR-21, miR-31, miR-128, miR-147 and miR-217 may be the important players in such interaction. [score:4]
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[+] score: 5
As shown in Figure 5b, VEGFA were targeted by the greatest number of the differential miRNAs, among which miR-429, miR-200b and miR-200c also interacted with VEGFC; in contrast, VEGFB was targeted only by miR-18a, miR-326, miR-330 and miR-128. [score:5]
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[+] score: 4
The death of specific cell types may explain the downregulation of microRNAs that are associated with neurons, such as miR-124 and miR-128 [48], and those associated with oligodendrocytes, such as miR-219, miR-138, and miR-338 [49], [50]. [score:4]
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[+] score: 4
Prominent among this group were miRNAs that are enriched in neurons and associated with developmental regulation (let-7i, let-7f, let-7b, miR-98), cell cycle regulation (miR-137, mIR-128) and neural activity (miR-132, miR-212). [score:4]
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[+] score: 4
In addition, miR-128-3p and -30e-3p were up-regulated both in the BMFC group and in the combined-supplement fed group. [score:4]
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[+] score: 3
For example, the JunB/miR-128/Foxo1 regulatory axis was shown to govern the development of lympathic vessels in zebrafish [29], whereas endothelial-specific ablation of JunB mediated by Tie-2 cre resulted in embryonic lethality at E10.5 with embryos exhibiting abnormal vascular structures [30]. [score:3]
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[+] score: 3
Other miRNAs from this paper: cel-let-7, cel-lin-4, 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-17, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, 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-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, hsa-mir-421, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-92b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Mouse miR-124a as well as miR-128, miR-101 and miR-132 have been reported to be expressed specifically in brain [15]. [score:3]
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[+] score: 2
A subsequent bioinformatic prediction suggested that 18 of these miRNAs play key roles during tooth development, including let-7f, miR-128, miR-200b and miR-200c [11]. [score:2]
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[+] score: 1
Therefore, we began this study with myocardin as the focus molecule and profiled four selected miRNAs, including miR-1, miR-9, miR-128 and miR-186 which were predicted by miRanda (http://www. [score:1]
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[+] score: 1
MiR-128, miR-132, miR-134, and miR-138 have also been shown to be involved in NSC maturation and dendritic spine morphogenesis [17]. [score:1]
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[+] score: 1
In addition, the neural progenitor cells isolated by LCM exhibited increases in miR-146a, miR-146b, miR-210, miR-19b and miR-378 and decreases in miR-128, miR-291a-3p, and miR-139-5p (Fig. 3A to 3C), which are consistent with the array data findings. [score:1]
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