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21 publications mentioning hsa-mir-576

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-576. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 213
However, at later stages of infection, miR-217 expression was already closer to uninfected expression levels (up-regulated only 1.7 at 12 h post-infection), whereas miR-576-3p was still up-regulated 2.83 times in infected cells, indicating a slightly different kinetics for those miRNAs. [score:11]
STING, the only one of the three selected targets of miR-576-3p that already demonstrated a significant down-regulation at 12 h post infection, showed an even higher down-regulation at 24 h post infection (39 fold down-regulation at 24 h post infection compared to 7.16 at 12 h post infection). [score:11]
To accomplish that, HuH-7 cells were transfected with non-human negative control miRNA inhibitor, miR-217 inhibitor, miR-576-3p inhibitor or both miRNA inhibitors and infected with OROV 3h post-transfection. [score:9]
We demonstrated that miR-217 and miR-576-3p were up-regulated during infection and that their cognate targets were down-regulated. [score:9]
The kinetics of expression of miR-217 suggests an early induction during infection compared to miR-576-3p, since miR-217 was up-regulated 2.26 times as early as 3 h post-infection while miR-576-3p was only up-regulated 1.44 at the same point. [score:8]
HuH-7 cells were transfected with 75 nM negative control inhibitor, miR-217 inhibitor, miR-576-3p inhibitor or both. [score:7]
0006508.g008 Fig 8HuH-7 cells were transfected with 75 nM negative control inhibitor, miR-217 inhibitor, miR-576-3p inhibitor or both. [score:7]
In order to validate the miRNAs that were significantly deregulated in the array (miR-26a-1-3p and miR-576-3p) and to verify the expression of the miRNAs only detected in infected cells in the expression profile array (miR-217, miR-26a-2-3p and miR-92a-1-5p), we designed specific primers for each miRNA and checked its expression by RT-qPCR (Fig 3). [score:7]
Negative control inhibitor, miR-217 inhibitor and miR-576-3p inhibitor (Integrated DNA Technologies) were transfected at a final concentration of 75 nM using 2 μl of Lipofectamine 2000 (Thermo Fisher Scientific) per replica. [score:7]
In order to evaluate if target regulation could present a higher effect in a later point of the infection, we selected two predicted and published targets for miR-217 and three for miR-576-3p to assess their expression 24 h post infection (Fig 6B). [score:6]
As most of those miRNAs are previously annotated as star miRNAs (as example of miR-26a-1-3p previously annotated as miR-26a-1*) and some prediction database algorithms use proved interaction as criteria for prediction, we only selected miR-217 and miR-576-3p, both mature strand miRNAs, for further target prediction analysis (one detected only in infected cells and the other one up-regulated significantly upon infection in the array, respectively, and both validated). [score:6]
However, as the infection proceed, the virus induces the miR-576-3p expression promoting the down regulation of its target genes STING and TRAF3 (Fig 7B and 7C)). [score:6]
To investigate possible pathways regulated by miR-217 and miR-576-3p during OROV infection, we performed target prediction using TargetScan, miRTarget2, PicTar, miRBase, TarBase and miRanda databases. [score:6]
At the same time point, two candidate targets, FGD4 and CAV2 were down-regulated, confirming the inverse trend of miR-576-3p (Fig 6A). [score:6]
Inhibition of miR-217 led to a 2.3 fold decrease in viral RNA replication, while inhibition of miR-576-3p led to a 7.7 fold decrease. [score:5]
Nonetheless, the predicted target genes for miR-217 and miR-576-3p, DCP2 and STING, respectively, recovered to similar levels to non-infected cells in the presence of miRNA inhibitors 18 h post-infection (Fig 8B). [score:5]
The highest reduction was observed with inhibition of both miRNAs (8.3 fold), but was not significantly lower than miR-576-3p inhibition alone (Fig 8C). [score:5]
Black columns represent predicted targets for miR-576-3p and gray columns represent predicted targets for miR-217, respectively. [score:5]
Our validation experiments showed the same tendency of the miRNAs panel with an increasing expression of both miR-217 (Fig 3A) and miR-576-3p (Fig 3B) during infection, reaching a peak of expression at 6 h post-infection (about 5.5 fold increase for both miRNAs). [score:5]
Furthermore, the inhibition of miR-217 and miR-576-3p partially restricted viral replication, as demonstrated by a decreasing in both viral RNA and titer in the presence of miRNA inhibitors (Fig 8). [score:5]
Ontology enrichment analysis [56] was performed for the predicted targets of the differentially expressed miR-217 and miR-576-3p. [score:5]
Relative expression levels of selected target mRNAs predicted for miR-217 and miR-576-3p. [score:5]
We demonstrated that miRNAs miR-217 and miR-576-3p, differentially expressed during infection, could be regulating crucial pathways, like innate immunity response, mainly in upstream proteins of interferon-β induction pathway (adaptor and kinase proteins, as well as transcription factors), protein shutoff and apoptosis. [score:4]
The three selected and unpredicted miR-576-3p targets, MAVS, TRAF3 and STING, are known to be important genes in the regulation of IFN-β response in viral infected cells [69]. [score:4]
Cellular target genes regulated by miR-217 and miR-576-3p. [score:4]
MiRNAs miR-324-3p (1.73x), miR-1227 (1.95x), miR-362-3p (1.85x), miR-99b-3p (2.21x), miR-19b-1-5p (4.11x), miR-628-3p (2.77x), miR-26a-1-3p (42.47x), miR-576-3p (2.49x) and miR-27a-5p (108x) were up-regulated, in OROV-infected cells relative to uninfected cells. [score:4]
The miR-576-3p expression peaked at 6 h post-infection and presented a kinetic similar to miR-217 (Fig 3B). [score:3]
Inhibition of miR-217 and miR-576-3p affects OROV replication. [score:3]
Black columns represent miR-217 expression levels and gray columns represent miR-576-3p levels. [score:3]
Finally, reduced viral titers confirmed the diminished replication, as a 3-fold decrease was observed in the same time point using miR-217 and miR-576-3p inhibitors (Fig 8D). [score:3]
The data suggest that both miR-217 and miR-576-3p could act synergistically to inhibit IFN-β antiviral response. [score:3]
Enrichment pathway analysis of predicted targets for miR-217 and miR-576-3p. [score:3]
Inhibition of miR-217 and miR-576-3p impairs OROV replication. [score:3]
Mean fold change of expression levels in OROV infected cells relative to uninfected cells for (A) miR-217 and (B) miR-576-3p. [score:3]
Those results are in accordance with previous data for miR-576-3p inhibition in other viral infections [69]. [score:3]
Network depicting the relation among miR-217, miR-576-3p and 92 selected target mRNAs found in at least 3 out 6 databases. [score:3]
When enough miR-576-3p accumulates in cytoplasm (6 h post-infection) the target mRNA levels, mainly for TRAF3 and STING, begin to fall progressively (Fig 7B and 7C)). [score:3]
Altogether, those data demonstrate that inhibition of miR-217 and miR-576-3p is a prospective approach to restrict OROV replication in HuH-7 cells. [score:3]
0006508.g005 Fig 5 Network depicting the relation among miR-217, miR-576-3p and 92 selected target mRNAs found in at least 3 out 6 databases. [score:3]
MiR-576-3p was recently proposed as a key miRNA in feedback regulation of IFN-β pathway in response to viral infections [69]. [score:2]
Moreover, IFN-β transcription regulation correlated with miR-576-3p, STING and TRAF3 transcription dynamics (Fig 7), implying in a temporal feedback mechanism in response to OROV infection, as suggested for other viruses. [score:2]
Concomitantly, miR-576-3p transcription is also activated by the transcription factor IRF3 and the miRNA accumulation increases until peak 6 h post-infection (Fig 3B). [score:1]
The miR-576-3p is a primate specific miRNA that was conserved along the evolution, presumably, to avoid tissue damage derived from an excessive inflammatory response due to an infection. [score:1]
We hypothesize that OROV try to escape IFN-β response reducing the levels of STING and TRAF3 through miR-576-3p induction (Fig 7D). [score:1]
From the thirteen selected miRNAs from the screening, only miR-576-3p and miR-26a-1-3p sustained significance (p ≤ 0.05, p ≤ 0.01, respectively) after Bonferroni correction according to the method used in this study. [score:1]
Our results suggested that, unlike mice, the presence of miR-576-3p in primates and repression of INF-ß rendered them more susceptible to OROV infection. [score:1]
miR-576-3p, IFN-β, STING and TRAF3 transcripts levels are represented by green, blue, red and yellow lines, respectively. [score:1]
We focused our analysis on miR-217 and miR-576-3p given the aforementioned reasons; nonetheless, we cannot exclude the possibility that the other miRNAs identified could be playing a role in OROV infection, as we could validated some of them (Fig 3C). [score:1]
We predicted 195 cellular genes to interact with miR-217, miR-576-3p, or both, using that criterion (S2 Table). [score:1]
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[+] score: 32
Amongst these 7 human miRNAs, 1 was up-regulated in OA chondrocytes (hsa-miR-483-5p) and 6 were up-regulated in normal chondrocytes in comparison to OA chondrocytes (hsa-miR-149*, hsa-miR-582-3p, hsa-miR-1227, hsa-miR-634, hsa-miR-576-5p and hsa-miR-641) (Figure 2 B and C). [score:7]
In this regard, hsa-miR-576-5p was down-regulated in OA chondrocyte pellets with the highest fold (4.74) whereas hsa-miR-483-5p was up-regulated in OA chondrocyte pellets with 2.44 fold. [score:7]
Amongst these 7 human miRNAs, 1 was up-regulated in OA chondrocytes (hsa-miR-483-5p) and 6 were up-regulated in normal chondrocytes (hsa-miR-149*, hsa-miR-582-3p, hsa-miR-1227, hsa-miR-634, hsa-miR-576-5p and hsa-miR-641). [score:7]
The number of transcription proteins obtained as putative mRNA targets regulated by hsa-miR-145, hsa-miR-576-5p and hsa-miR-1227 were also high (18% to 19%), whereas secretory, membrane, surface or receptor proteins as predicted targets regulated by hsa-miR-149, hsa-miR-483-5p, hsa-miR-582-3p, hsa-miR-634 and hsa-miR-641 were also elevated (15 to 19%). [score:7]
It is noteworthy that some of the miRNAs differentially expressed in chondrocyte that we identified in our study are novel as compared with those identified and published in the literature, e. g. hsa-miR-576-5p, hsa-miR-582-3p, hsa-miR-634, hsa-miR-641, hsa-miR-1227, suggesting that they may therefore represent new targets in articular cartilage. [score:4]
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[+] score: 19
Anti miR-576-3p treatment resulted in the upregulation of AP1G1 while pre miR-576-3p suppressed its expression. [score:8]
One of the ways which the Influenza virus enters the host cells is via clathrin -mediated endocytosis, thus regulating AP1G1 expression with miR-576-3p could affect the viral entry into cells for we observed miR-576-3p to be a repressor of AP1G1 expression. [score:6]
miR-576-3p was not detectable in exosomes, while miR-26a and miR-628-3p were upregulated in exosomes. [score:4]
The anti miRNAs and miRNA mimics used in this study are commercially available (Anti/Mimic miR-26a (MH/MC10249), Anti/Mimic miR-576-3p (MH/MC13069), Anti/Mimic miR-628-3p (MH/MC12299); Ambion, USA). [score:1]
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[+] score: 8
Since IRF3 is a downstream signalling molecule in the STING-TBK1 axis, upregulation of miR-576-3p serves as a negative feedback loop to prevent sustained inflammatory response during and post infections. [score:4]
Further studies show that miR-576-3p is an IRF3 -induced gene that can target multiple genes of interferon-stimulators, including STING, MAVS, TRAF3 and STAT6, thereby reducing their levels [119]. [score:3]
In a negative feedback loop, the product of the IRF3 -dependent antiviral response, microRNA-576-3P (miR-576-3P), can prevent further STING activation. [score:1]
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[+] score: 8
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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
A panel of five circulating miRNAs was observed to be upregulated in serum samples from infected patients (miR-202, miR-342-5p, miR-206, miR-487b, and miR-576-5p), showing high sensitivity and specificity for differentiation of pertussis patients and HC. [score:4]
Further analyses showed that six of these miRNAs (miR-1260, miR-335*, miR-664, miR-26a, miR-576-3p, and miR-628-3p) had similar expression signatures in human A549 and Madin–Darby canine kidney (MDCK) cells infected with H1N1 in vitro. [score:3]
In addition, examination of MDCK supernatant exosomes indicated that only miR-576-3p was not detectable (218). [score:1]
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[+] score: 8
Previous studies have demonstrated that rifampin also inhibited anti-angiogenesis by regulating the expression of multiple miRNAs (miR-34b, miR-886-3p, miR-218, miR-576-3p, miR-200c, miR-616, miR-660, miR-335, miR-92a), and further induced the gene expression of BIRC3, CAV1, CAV2, FN1, ITGA1 and THBS1. [score:8]
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[+] score: 7
detected the expression profile of miRNAs from blood samples of influenza A H1N1 virus-infected patients and then exhibited that the expression levels of 193 miRNA molecules were altered in all influenza patients, of which 16 highly dysregulated miRNAs (miR-1260, miR-1285, miR-18a, miR-185*, miR-299-5p, miR-26a, miR-30a, miR-335*, miR-34b, miR-519e, miR-576-3p, miR-628-3p, miR-664, miR-665, miR-765 and miR-767-5p) were able to provide a clear distinction between infected and healthy individuals [39]. [score:6]
A combination of the serum levels of miR-361-5p, miR-889 and miR-576-3p were shown to distinguish pulmonary tuberculosis patients from healthy individuals [26]. [score:1]
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[+] score: 7
Their results included two of the most upregulated (miR-221 and miR-222) and six downregulated miRNAs (miR-151-3p, miR-19a, miR-20b, miR-342-3p, miR-363, and miR-576-3p). [score:7]
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[+] score: 6
In comparison with uninfected reads, highly expressed aae-mir-23, aae-mir-576 and aae-mir-320 were upregulated in CHIKV-infected Ae. [score:6]
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[+] score: 5
MiRNA target site/Species Human Mouse Cow Dog Chicken FrogTargeting Twist2 miR-15b-3p + − + + − − − miR-33-5p + + + + − + − miR-137-3p + + + + − + − miR-145a-5p + + + + − − + miR-151-5p + + + + − + − miR-214-5p + + + + − − − miR-326-3p + + + + − − − miR-337-3p + + + + − + − miR-361-5p + + + + − − − miR-378a-5p + + + + − − − miR-381-3p + + + + − + − miR-409-3p + + + + − − − miR-450b-5p + + + + − + − miR-508-3p + + + + − − − miR-543-3p + + + + − − − miR-576-5p + + + + − − − miR-580 + + + + − − − miR-591 + + + + − − − MicroRNAs underlined were tested in this study. [score:5]
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[+] score: 5
Our previous studies have identified various miRNAs functioning as tumor suppressors in bladder cancer, including miR-101, miR-124-3p, miR-320c, miR-433, miR-409-3p, miR-490-5p, and miR-576-3p, which regulate the proliferation, migration and invasion of bladder cancer cells by down -regulating various oncogenes [17– 23]. [score:5]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Indeed, although CTNNA2 can be regulated by primate-specific miRNAs common to both monkeys and humans (miR-513a-3p, miR-518a-5p, miR-548a-5p, miR-576-5p, miR-586, miR-607, miR-625, miR-642), a number of miRNAs present in Homo sapiens but not in Macaca mulatta (miR-1208, miR-1247, miR-1290, miR-1324, miR-1825, miR-613 and miR-634) also target CTNNA2 [19], [29]. [score:4]
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[+] score: 4
As this table demonstrates, some miRNAs, such as miR-576-5p, had a median expression close to the background. [score:3]
The most significant miRNA hsa-miR-576-5p reached an adjusted significance value of 4.7 × 10 [−16] (raw P =5.6 × 10 [−19]). [score:1]
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[+] score: 4
MiRNA-144 was found to be highly expressed in the PBMC compared to miRNA-361-5P, miRNA-889, and miRNA-576-3p that were significantly down regulated in active tuberculosis patients. [score:3]
However, increased level of miRNA-361-5p, miRNA-889, and miRNA-576-3p have been reported in tuberculosis infected serum as non-invasive molecular biomarker for rapid diagnosis and prevention of tuberculosis infection (Qi et al., 2012). [score:1]
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[+] score: 4
Amongst the 7 miRNAs (miR-483-5p, miR-149, miR-582-3p, miR-1227, miR-634, miR-576-5p, and miR-641) detected by Silvia Díaz-Prado1 et al., 6 miRNAs were down-regulated in OA chondrocytes, and miR-634 is one of the six miRNAs 16. [score:4]
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[+] score: 4
A microarray -based, large-scale analysis identified the signatures of six miRNA, of which levels are increased in normal chondrocytes of human origin relative to OA chondrocytes (miRNA-1227, miRNA-576-5p, miRNA-149*, miRNA-634, miRNA-641, and miRNA-582-3p) and a single miRNA, namely miRNA-483-5p, which is selectively up-regulated in OA chondrocytes [108]. [score:4]
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[+] score: 3
It was observed that in whole blood of H1N1 patients, miR-1260, miR-26a, miR-335, miR-576-3p, miR-628-3p and miR-664 are differentially expressed [57]. [score:3]
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[+] score: 3
Similarly, of 46 suppressed miRNAs, we recognized 14 human-specific non-homologous miRNAs, including miR-1206, miR-548a-5p, miR-548f, miR-576-5p, miR-600, miR-639, miR-640, miR-641, miR-647, miR-662, miR-886-3p, miR-887, miR-628-3p, and miR-888. [score:3]
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[+] score: 3
A set of three miRNAs, i. e. miR-361-5p, miR-889, and miR-576-3p, was identified that specifically indicated TB disease. [score:3]
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[+] score: 2
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
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[+] score: 1
We focused our analysis on 12 miRNAs (miR-22, miR-29a-3p, miR-34a, miR-126, miR-140-3p, miR-141, miR-181c-5p, miR-202, miR-455-5p, miR-508-3p, miR-517a-3p and miR-576-3p). [score:1]
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