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17 publications mentioning gga-mir-15a

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-15a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 275
In this study, we identified the influence of long-term hypoxia stress on lung development and showed that the miR-15a, downregulation of HIF-1, was responsive to the oxygen concentration and induced mesenchymal ablation through direct inhibition of the antiapoptotic gene chicken bcl-2 by binding to a unique target region. [score:10]
bcl-2 is a target gene of miR-15a but not miR-16 in chicken lung tissues under hypoxiamiR-15a and miR-16 negatively regulate bcl-2 by directly binding to a particular sequence in the 3′-UTR of bcl-2 and inhibiting its translation [21], [31]. [score:9]
Our observation of hypoxia -induced miR-15a expression (Fig. 1B) and reduced Bcl-2 protein levels at E19 (Fig. 2C) indicated an inverse relationship between miR-15a and Bcl-2 protein expression, which suggested a causative role for miR-15a in the downregulation of bcl-2. However, as a cluster member of miR-15a, miR-16 was identified as hypoxia insensitive. [score:8]
Taken together, these results suggested that the lung appeared resistant to apoptosis at E18, which is likely the result of upregulation of Bcl-2. However, at E19, the time of further lung development, the tissues became more sensitive to the oxygen concentration, and apoptosis was induced by the hypoxia -induced upregulation of miR-15a. [score:8]
To our knowledge, our work is the first to document that chicken miR-15a, but not miR-16, regulates apoptosis by directly targeting chicken bcl-2 at a specific target region during later chick lung CCGS development. [score:8]
miR-15a and miR-16, two members of the miR-15a/16 cluster, play a role in proapoptosis regulation by inhibiting the translation of the antiapoptotic protein Bcl-2 via binding to the 3′-untranslated region (3′-UTR) of bcl-2 mRNA [21]. [score:8]
miR-15a and miR-16 negatively regulate bcl-2 by directly binding to a particular sequence in the 3′-UTR of bcl-2 and inhibiting its translation [21], [31]. [score:7]
Hypoxia stress induces proapoptotic chicken miR-15a expression and subsequently inhibits the translation of the antiapoptotic protein Bcl-2, resulting in mesenchyme ablation. [score:7]
To determine whether both miR-15a and miR-144 are highly expressed throughout chicken embryonic development or just a temporally variable expression pattern, we compared the miR-15a and miR-144 expression profiles in lung tissues. [score:7]
In later stages of chick embryo development, relatively strong expression of miR-15a and miR-144 was detected in lung tissues with Northern blotting, whereas expression was weak in other organs (Fig. 1A). [score:6]
We also showed that only miR-15a and not miR-16 was responsive to the oxygen concentration and induced mesenchymal ablation through direct inhibition of the antiapoptotic gene chicken bcl-2 by binding to a unique target region. [score:6]
In the present study, we detected upregulation of both HIF-1 and miR-15a with a similar expression profile during E16–E19. [score:6]
In human tumors, E2F1 is a positive regulator of miR-15a and miR-16, but only miR-15a inhibits expression of cyclin E [81]. [score:6]
We also co -transfected these cells with chicken miR-15a mimic, mimic and inhibitor, or mimic control (miRNA mimics are small, chemically modified double-stranded RNAs that mimic endogenous miRNAs and enable miRNA functional analysis by up-regulation of miRNA activity. [score:6]
In a mouse mo del of ischemia -induced cerebral injury, PPARδ (peroxisome proliferator-activated receptorδ) was identified as a regulator of miR-15a that inhibits the induction of apoptosis by preventing miR-15a expression [22]. [score:6]
Together, our experimental data extend these early findings and further show that chicken miR-15a can repress bcl-2 translation by directly binding to the 3′-UTR of bcl-2 with a different target site sequence. [score:6]
Although miR-15a and miR-16 belong to the same cluster and miRNA family, Yin et al. also reported that miR-15a plays a causative role in the regulation of apoptosis by directly targeting bcl-2 during ischemic vascular injury [22]. [score:5]
To determine whether the peak value of miR-15a expression was lung specific or was a systemic reaction to hypoxia and whether expression of miR-15a was the same as that of miR-16, we performed real-time PCR for miR-15a and miR-16 using chick embryo lung, heart, brain and liver at E16 and E19. [score:5]
Comparing the expression levels at E20, we found that expression of miR-15a was relatively low in both tissues under normal conditions (nT, nW chickens), and relatively high in the hW and hT sample which incubated under plateau simulating condition (Fig. 1B). [score:5]
0098868.g006 Figure 6(A) In chicken lung, hypoxia stress stimulates gga-miR-15a expression, and miR-15a may bind to the 3′-UTR of gga- bcl-2 and inhibit its antiapoptotic activity through posttranscriptional gene silencing. [score:5]
In co -transfected cells, the miR-15a mimic decreased the expression of hRluc and miR-15a mimic inhibitor rescued hRluc activity; no differences were seen for miR-16. [score:5]
The RNA22/PicTar results showed that the target site sequence complemented only with chicken miR-15a, and the TargetScan result suggested that both the chicken miR-15a and miR-16 would work (data not shown). [score:5]
At E18, the hT group showed significant upregulation of miR-15a that remained relatively high and stable through d3 (Fig. 1B). [score:4]
Together, the results suggested that chicken miR-15a decreased chicken bcl-2 translation by directly acting on a miR-15a–specific response element in the 3′-UTR of chicken bcl-2 mRNA and that this effect may be different in chicken bcl-2 as compared with that in human bcl-2. Chicken miR-16, another member of the cluster, did not affect bcl-2 regulation. [score:4]
At E19, the time at which the respiratory CCGS develops, miR-15a was also upregulated in hW and nT chickens. [score:4]
We hypothesize that the induced ablation of mesenchymal cells may involve HIF-1 as a hypoxia sensor, which then indirectly decreases Bcl-2 protein levels by inducing miR-15a expression. [score:4]
Therefore, either inhibition of miR-15a or activation of HIF-1 or Bcl-2 may potentially be therapeutic options for preventing hypoxia -induced lung damage and may reduce death at particular stages of chick embryo development. [score:4]
To further verify whether miR-15a or miR-16 repressed chicken bcl-2 by binding directly to the predicted binding site in its 3′-UTR as shown in human cells [31], we analyzed the complementation of the chicken bcl-2 mRNA (NM_205339.1) and chicken miR-15a/16 using four different prediction algorithms: TargetScan [33], RNA22 [34], DIANA [35], [36], and PicTar [37]. [score:4]
We note that miR-15a expression was increased at E19 during hypoxia (Fig. 1B). [score:3]
In this study, we suppose that in chick, members of the miR-15a/16-1 cluster respond to hypoxia through different target genes and pathways. [score:3]
miR-15a in hW showed continuously increasing expression from E18 and a peak at E20 and the hatch out day (d1) (Fig. 1B). [score:3]
hW showed remarkable upregulation of miR-15a at E19 as compared with that at E16 in the embryonic lung (Fig. 1C). [score:3]
miR-709 responds to apoptosis stimuli and prevents expression of miR-15a/16 in mouse [77]. [score:3]
bcl-2 is a target gene of miR-15a but not miR-16 in chicken lung tissues under hypoxia. [score:3]
As a control, miR-15a in nT chickens showed a relatively smooth line, indicating stable, low expression of miR-15a (Fig. 1B). [score:3]
Xu and colleagues [26] published that the expression levels of both miR-15a and miR-144 are higher in the lung tissue. [score:3]
We also found differences in hypoxia -induced expression of miR-15a and miR-16 between high-altitude and plain chicks. [score:3]
miR-15a and the binding site in the gga- bcl-2 3′-UTR are shown, but miR-16 shows no target site in this part of the sequence. [score:3]
In the heart and brain, miR-15a expression in hW and hT was also increased from E16 to E19, but the range was not as large as that in the lung (Fig. 1C). [score:3]
Particular transcriptional factors (TF) may respond to the hypoxia stress and induce gga-miR-15a expression. [score:3]
Thus, miR-15a expression was sensitive to oxygen concentration, and the strongest response was detected in lung tissue. [score:3]
Chicken miR-15a decreased luciferase activity of the reporter vector containing the 3′-UTR sequence, and the level of luciferase activity recovered in the presence of the chicken miR-15a inhibitor. [score:3]
The expression of miR-15a and miR-144 is induced by hypoxia stress in chicken embryo. [score:3]
Other molecules have been reported as miR-15a regulators in different cell types or tissues, and some are hypoxia regulated. [score:3]
Under hypoxia stress, miR-15a was more highly expressed at E19 than at E16 in the brain, heart and lung for the hW group and in the lung and brain for the hT group. [score:3]
The psiCHICK-2 vector was transfected into the human embryonic kidney 293T cells with miR-15a/16 mimics (Applied Biosystems) or a miR-15a/16 inhibitor (Applied Biosystems) or a negative control (Applied Biosystems). [score:3]
In this study, our data suggested that the expression of miR-15a, but not miR-16, is sensitive to the oxygen concentration and was significantly increased in lung mesenchymal cells in chicken. [score:3]
Hypoxia -induced miR-15a overexpression promotes the formation of CCGS and a thin BGB. [score:3]
Expression of miR-15a in nW chickens nearly coincided with that of nT chickens except for a relative peak value for nW at E19 (Fig. 1B). [score:3]
A comparison of interclass differences showed that at E18, expression of miR-15a was higher in lung tissues from hT than in the lung tissues from the other three groups. [score:3]
The miR-15a binding site in the bcl-2 3′-UTR sequence mediates translation repression by miR-15a. [score:3]
Real-time PCR showed no difference in miR-15a and miR-144 expression from E13 to E17 in the four groups (data not shown). [score:3]
bcl-2 is a target gene of miR-15a, but not miR-16 in chicken lung. [score:3]
0098868.g003 Figure 3 bcl-2 is a target gene of miR-15a, but not miR-16 in chicken lung. [score:3]
The inhibition of miR-15a or activation of HIF-1 or Bcl-2 may prevent hypoxia -induced lung damage and reduce chick embryo death. [score:3]
At E19 of the nW chicken group, the expression of miR-15a remained relatively high in the hT chicken group compared with the nT, nW chicken groups and was largely unchanged in the nT chicken group through the whole embryo stages. [score:2]
To further understand a possible role for hypoxia -induced miR-15a in the development of a functional lung in vivo, we immunostained sections from hT, hW, nT, and nW chicken lungs for Bcl-2 protein and performed terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining. [score:2]
We also show that of the two cluster and family members, only chicken miR-15a is responsive to hypoxia stress and participates in downstream regulation. [score:2]
HERΔ16, a clinically important oncogenic isoform of HER2, is another regulator of miR-15a/16 in breast tumors [80]. [score:2]
In conclusion, the mechanisms of hypoxia -induced, miR-15a–mediated CCGS and thin BGB establishment are important for understanding adaptational development of chick lung at particular stages. [score:2]
Myc and HDAC3 are regarded as miR-15a/16 regulators in mantle cells and other non-Hodgkin B-cell lymphomas [78], [79]. [score:2]
Schematic representation of hypoxia -induced gga-miR-15a control of mesenchymal cell death/ablation during functional lung establishment and adaptive development. [score:2]
HIF-1 may regulate miR-15a in this setting. [score:2]
We cloned the entire chicken bcl-2 3′-UTR, containing the miR-15a/16 binding site, and inserted it into the multiple cloning sites of the psiCHICK-2 vector. [score:1]
Chicken bcl-2 was predicted to contain a miR-15a/16: bcl-2 site located at nt 369–390 of its 3′-UTR (Fig. 3A). [score:1]
As a cluster and family member, miR-16 was reported to have the same function as miR-15a [21]. [score:1]
Kang et al. [66] reported that the miR-15a/16-1 cluster is a homo-cluster. [score:1]
0098868.g001 Figure 1(A) Total RNA from tissues from E19 chicken embryos was blotted with probes for miR-15a, miR-144 and U6 (loading control). [score:1]
Hybridization was done using the 5′-digoxigenin–labeled miRCURY LNA microRNA Detection Probes anti-gga-miR-16 and anti-gga-miR-15a (EXIQON, Vedbaek, Denmark). [score:1]
Although miR-16 belongs to the same cluster and family as miR-15a [21], they were differentially sensitive to hypoxia. [score:1]
Chicken miR-16, a cluster and family member of chicken miR-15a, does not affect the hypoxia -induced pathway. [score:1]
In contrast, Cimmino et al. showed that miR-15a and miR-16 promote apoptosis by posttranscriptional gene silencing of bcl-2 [21]. [score:1]
miR-15a and miR-144 were identified in late-stage embryonic lung tissue. [score:1]
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[+] score: 90
Other miRNAs from this paper: gga-mir-16-1, gga-mir-16-2, gga-mir-16c
Based on this combined information, we inferred that gga-mir-15a could target FOXO1 by binding to the 3′-UTR of FOXO1 mRNA and then inhibit the protein expression of FOXO1 involved in the insulin-signaling pathway, resulting in the alteration of FCR in chickens. [score:7]
As an important independent regulatory molecule, microRNA-15a is involved in the regulation of cell apoptosis and proliferation [19], autoimmunity disease [20, 21], cardiovascular disease [22] and insulin synthesis [23]. [score:7]
TargetScan and miRDB software was used for target gene prediction for gga-miR-15a, and a total of 196 and 363 (target score ≥ 80) genes were predicted using these two tools, respectively (Additional file 1: Tables S2 and S3). [score:7]
In this study, based on the molecular interaction analysis, FOXO1 was identified as the most reliable target gene of gga-mir-15a among 12 target genes. [score:5]
Predicted target genes from TargetScan for gga-mir-15a. [score:5]
Therefore, we used the bioinformatics tools to predict and analyze the target genes of gga-miR-15a, and twelve target genes of gga-miR-15a were significantly enriched in the insulin-signaling pathway. [score:5]
The expression of MIR15A was significantly lower in the medium and low FCR birds, which suggested that MIR15A was a promising candidate gene involved in the regulation of FCR. [score:4]
The interactions between MIR15A and target genes, such as FOXO1, suggested that the insulin-signaling pathway in the liver might be the causative factor affecting FCR regulation in chickens. [score:4]
Sun et al. [23] previously demonstrated that microRNA-15a positively regulated insulin synthesis by targeting uncoupling protein-2 (UCP-2) in mice. [score:4]
Fig. 4Expression of gga-mir-15a for hens with high, medium and low feed conversion ratio. [score:3]
Bioinformatics analysis further revealed that gga-mir-15a could act on many target genes, such as forkhead box O1 (FOXO1) that is involved in the insulin-signaling pathway, which influences nutrient metabolism in many organisms. [score:3]
Predicted target genes from miRDB for gga-mir-15a. [score:3]
Molecular interactions between gga-mir-15a and target genes with minimal free energy less than −20 kcal/mol. [score:3]
of quantitative real-time polymerase chain reaction (qRT-PCR) analysis in liver tissue showed that the expression of gga-miR-15a was significantly higher in the high FCR birds than that in the medium or low FCR birds. [score:3]
We found that the relative expression of gga-miR-15a was significantly higher in the HFCR group than that in MFCR and LFCR groups (Fig. 4b), suggesting that the gga-miR-15a should be a promising candidate gene for feed efficiency. [score:3]
Target gene prediction for gga-miR-15a. [score:3]
A total of 9 interactions were found between gga-miR-15a and three target genes with an MFE less than −20. [score:3]
b Expression of gga-mir-15a for the selected hens. [score:3]
Expression of gga-miR-15a in liver tissue. [score:3]
These 3 genes were forkhead box O1 (FOXO1), 3-phosphoinositide dependent protein kinase 1 (PDPK1) and protein kinase cAMP -dependent type II regulatory subunit alpha (PRKAR2A) (Additional file  4: Figure S3), and the lowest MFE was found between gga-miR-15a and FOXO1, which showed two binding sites with −28 and −24.6 kcal/mol MFE (Fig.   5). [score:2]
Feed efficiency Gga-miR-15a Late laying period Chickens People are always paying attention to animal feed efficiency because of the large effect on farm profitability. [score:1]
Gga-miR-15a (MIR15A) was the only gene near these 3 genome-wide significant loci. [score:1]
According to the genome of vertebrates, MIR15A, accompanied by MIR16–1 and DELU2 nearby, forms a DLEU2/miR-15a/16–1 cluster to affect chronic lymphocytic leukemia in cancer research [17, 18]. [score:1]
a) Plot for feed conversion ratio, b) Plot for daily feed intake, c) Plot for residual feed intake Table 3 The information for SNPs associated with feed intake and efficiency traitsTraits [a] SNPGGA [b] Position P-value [c] MAF [d] β [e] Candidate/nearest geneLocation (kb) [f] FCR rs13553102 1 168,708,318 2.35e-7* 0.41 (A/G) −0.29 MIR15A U 13.57 rs314376310 1 168,738,343 7.93e-7* 0.51 (G/C) −0.29 MIR15A U 43.57 rs13972109 1 168,739,928 1.27e-6* 0.50 (T/C) −0.28 MIR15A U 45.16 FI rs313839239 9 4,521,384 6.21e-6 0.06 (T/C) 0.56 FARP2 Intron 1 rs313750381 9 4,358,988 2.47e-5 0.04 (A/G) 0.59 KIF1A Intron 22 rs314936159 9 4,371,299 2.47e-5 0.04 (A/G) 0.59 KIF1A U 0.59 rs313292633 9 4,397,583 2.47e-5 0.04 (T/C) 0.59 SNED1 Exon 11 rs312606176 9 4,402,911 2.47e-5 0.04 (G/A) 0.59 SNED1 Intron 22 RFI rs314723494 3 75,533,793 1.94e-5 0.33 (T/C) 3.17 CNR1 U 46. [score:1]
The SNP was located at 13.55 Kb upstream of MIR15A with a MAF of 0.41. [score:1]
FI and RFI denote daily feed intake and residual feed intake, respectively According to the association analysis of FCR, all genome-wide significant SNPs were near gga-miR-15a. [score:1]
Linkage disequilibrium (LD) and conditional GWA analysis indicated that these 3 SNPs were highly correlated with one another, located at 13.55–45.16 Kb upstream of gga-miR-15a. [score:1]
Additionally, gga-mir-15a (MIR15A) was in this region and close to the three significant SNPs. [score:1]
The cDNA was used to run quantitative real-time PCR (qRT-PCR) for gga-miR-15a. [score:1]
Green letters indicate the matured sequences of gga-miR-15a. [score:1]
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[+] score: 26
Other miRNAs from this paper: gga-mir-16-1, gga-mir-16-2, gga-mir-16c
MicroRNA-15a positively regulates insulin synthesis by inhibiting uncoupling protein-2 expression. [score:5]
In addition, one other microRNA, MIR15A, is also known to be an important independent regulatory molecule involved in the control of cell proliferation and apoptosis, cardiovascular and autoimmune diseases, and the synthesis of insulin (Andersen et al., 2010; Sun et al., 2011; Yuan et al., 2012; Spinetti et al., 2013). [score:4]
During chick embryonic development, the inhibition of MIR15A or the activation of HIF-1 or Bcl-2 can prevent hypoxia -induced lung damage and reduce the number of chick embryonic deaths (Hao et al., 2014). [score:4]
Yuan et al. (2017) noted that MIR15A can also control the feed conversion ratio in laying chickens and exerts an influence on a number of target genes, including forkhead box O1 (FOXO1) which is also involved in the insulin-signaling pathway (Yuan et al., 2017). [score:3]
Hypoxia -induced miR-15a promotes mesenchymal ablation and adaptation to hypoxia during lung development in chicken. [score:2]
Detailed information regarding the genes identified in this study is summarized in Table 3; one candidate was deleted in lymphocytic leukemia 7 (DLEU7), a microRNA (MIR15A) was detected adjacent to significant SNPs, and we also identified several genes near to suggestively significant SNPs, including the ribonuclease H2 subunit B (RNASEH2B), a potassium channel regulator (KCNRG), and a SPRY domain containing 7 (SPRYD7). [score:2]
This pathway stimulates protein synthesis and cell growth via mTOR signal activation (Kim et al., 2002); we therefore suggest that MIR15A has an indirect effect on longitudinal EW by affecting the deposition of egg white and yolk. [score:2]
Role of microRNA-15a in autoantibody production in interferon-augmented murine mo del of lupus. [score:1]
Conditional GWAS and LD analyses at EW36 revealed SNPs that are closely linked together within this significant genomic region; the annotation of significant SNPs shows that one candidate gene, DLEU7, and a promising microRNA (MIR15A) around this region are both also associated with EW36. [score:1]
MicroRNA-15a and microRNA-16 impair human circulating proangiogenic cell functions and are increased in the proangiogenic cells and serum of patients with critical limb ischemia. [score:1]
Genome-wide association study reveals putative role of gga-miR-15a in controlling feed conversion ratio in layer chickens. [score:1]
[1 to 20 of 11 sentences]
[+] score: 25
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-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
In addition the miRNAs clusters that were significantly down-regulated miR-15/16 and let-7 are typically down-regulated in stem cells and cancer [62- 64]. [score:7]
Clusters mir-16-1-mir-15a, let-7f-let-7a-1, mir-181a-1-mir-181b-1, let-7j-let-7k, mir-23b-mir-27b-mir-24, and mir-16-2-mir-15b were down-regulated in lungs and mir-181a-1-mir-181b-1 was also down-regulated in tracheae with AIV infection. [score:7]
Based on other immune related miRNA studies in mammals [11, 66], differentially expressed miRNAs of their mammalian homologs and their targets are presented in Table 9. MiR-15a, miR-21 and miR-181a have important functions in lymphocytes development and modulations while miR-122 and miR-24 are related to virus infection and miR-146a, induced by macrophages, can activate Toll like receptor (TLR) and expose antigens to interleukin-1 beta. [score:6]
The miRNAs from five of these clusters (mir-16-1-mir-15a, mir-16-2-mir-15b, let-7f-let-7a-1, let-7j-let-7k and mir-23b-mir-27b-mir-24) identified in both lungs and tracheae were significantly down-regulated in infected lungs compared to non-infected lungs and also had higher expression levels in non-infected lungs than non-infected tracheae. [score:5]
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[+] score: 23
Other miRNAs from this paper: gga-mir-16-1, gga-mir-16-2, gga-mir-15b, gga-mir-15c, gga-mir-16c
These two microRNAs, gga-miR-15a and gga-miR-16-1, were known to target some key genes such as B-cell leukemia/lymphoma 2 to regulate tumor growth [30], [31]. [score:4]
Green letters indicate the matured sequences of gga-miR-15a or gga-miR-16-1. Combining results of RNA analysis and association analysis, the 3 Mb region of 172–175 Mb with 63 coding genes and two microRNA genes likely contained more than one causal mutations affecting chicken growth and could contain a gene regulatory mechanism. [score:3]
These results indicated some specificity of RNA targeting to FOXO1A and KPNA3 by gga-miR-15a and gga-miR-16-1. 10.1371/journal. [score:3]
Green letters indicate the matured sequences of gga-miR-15a or gga-miR-16-1. Combining results of RNA analysis and association analysis, the 3 Mb region of 172–175 Mb with 63 coding genes and two microRNA genes likely contained more than one causal mutations affecting chicken growth and could contain a gene regulatory mechanism. [score:3]
These results indicated some specificity of RNA targeting to FOXO1A and KPNA3 by gga-miR-15a and gga-miR-16-1. 10.1371/journal. [score:3]
Insulin-like growth factor 1 (IGF1) gene, which involved in mediating growth and development, had a conserved binding site with miR-15 and miR-16 family in human [32], [33]. [score:2]
Both gga-miR-15a and gga-miR-16-1 could bind to the mRNAs of FOXO1A and KPNA3 (MFE = −28 and −28.9 for FOXO1A and MFE = −24.3 and −22.9 for KPNA3, Figure 3). [score:1]
The results showed that chicken IGF1 had a conserved binding site with gga-miR-15a and gga-miR-16-1 (MFE = −24.1 and −23.9, Figure 3). [score:1]
The 1.5 Mb region of KPNA3- FOXO1A could be immediate interest for candidate genes that may include FOXO1A, KPNA3, INTS6, gga-miR-15a, gga-miR-16-1 and RNASEH2B. [score:1]
The two microRNA genes, gga-miR-15a and gga-miR-16-1, approximately were in 300 Kb∼1 Mb distances to the five most significant SNPs in the 1.5 Mb region. [score:1]
Green letters indicate the matured sequences of gga-miR-15a or gga-miR-16-1. in this study identified novel candidate genes in a 3 Mb GGA1 region and provided strong confirmation of some previously reported QTL effects. [score:1]
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[+] score: 21
Other miRNAs from this paper: gga-mir-16-1, gga-mir-16-2, gga-mir-15b, gga-mir-15c, gga-mir-16c
After transfection in DF-1 chicken embryo fibroblast cells and 36 h of culture, the mature miR-16 expression in the insertion types was significantly lower than that in the deletion types (p <  0. 01), while mature miR-15a expression exhibited little changes (Fig. 3E). [score:5]
Expression analysis revealed that miR-16 expression in the muscle tissue of birds with the homozygous deletion type (low-weight line, n = 4) was much higher than that in the homozygous insertion type (high-weight line, n = 4) (Fig. 1D), while miR-15a showed no significant change (not show), which is consistent with our liver transcriptomic data. [score:5]
To determine the relationship between the mutation and miRNA expression level, real time PCR was performed to detect mature miR-15a and miR-16. [score:4]
Forty-six genes and miR-15a/16 were successfully detected (Fig. 1A), of which three genes (SUCLA2, CKAP2 and miR-16) exhibited significantly decreased expression in the high weight lines. [score:3]
Although miR-15a and miR-16-1 are produced from the same primary cluster, the expression levels vary. [score:3]
Five types of alternative splicing sites were detected in the insertion individuals without 5′ terminal splicing of mature miR-16, while 3 types of normal alternative splicing sites were detected in the 5′ terminal of mature miR-15 and miR-16 for the deletion individuals (Fig. 3A; Supplementary Table S4). [score:1]
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[+] score: 13
In addition, miR-15 and miR-16 are negatively correlated with expression of the anti-apoptotic gene BCL-2 [25], which inhibits apoptosis at the level of the mitochondria and is critical for cancer cells [26]. [score:5]
Calin G. A. Dumitru C. D. Shimizu M. Bichi R. Zupo S. Noch E. Aldler H. Rattan S. Keating M. Rai K. Frequent deletions and down-regulation of micro -RNA genes miR15 and miR16 at 13Q14 in chronic lymphocytic leukemia Proc. [score:4]
Cimmino A. Calin G. A. Fabbri M. Iorio M. V. Ferracin M. Shimizu M. Wojcik S. E. Aqeilan R. I. Zupo S. Dono M. MiR-15 and miR-16 induce apoptosis by targeting BCL2 Proc. [score:3]
MiR-15 and miR-16 are located in the 13q14 chromosome region, the partial absence of which was strongly influential in an outbreak of chronic lymphocytic leukemia (CLL). [score:1]
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[+] score: 12
All members of the miR-15, miR-181, and miR-29 families were down-regulated in L30 compared with L20, whereas the other families included members that were either up- or down-regulated. [score:6]
MiR-101-3p (−2.1-fold) and miR-15c-5p (−1.4-fold) had the most target genes followed by miR-15a, miR-16-5p, miR-214, miR-16c-5p, and miR-181b-5p (Supplementary Table S4), and these miRNAs were all down-regulated in L30 compared with L20. [score:5]
Seven conserved families all were DE with P ≤ 0.05, including let-7 (let-7a, -7b, -7c,-7f, -7g, -7i, -7j, and -7k), miR-130 (miR-130a, and -130b), miR-146 (miR-146a, -146b, and -146c), miR-15 (miR-15a, -15b, and -15c), miR-181 (miR-181a and -181b), miR-29 (miR-29a, -29b and -29c), and miR-30 (miR-30a, -30b, -30c, -30d, and -30e). [score:1]
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[+] score: 11
In mammals, a number of miRNAs have been demonstrated to target genes involved in adipogenesis and lipid metabolism, such as the regulation on the proliferation of adipose tissue-derived mesenchymal stem cells by miR-21 and miR-196a [4– 6]; the enhancement of adipogenesis by miR-103, miR-224 and the miR-17–92 cluster [7– 9]; the impairment of adipogenesis by the let-7 family, miR-448, miR-15a and miR-27 [10– 13]; the regulation of adipocyte lipid metabolism by miR-27a and miR-143 [13– 15]; and the important role of miR-33 on the repression of sterol transporters reported in numerous studies [16– 24]. [score:5]
miR-15a can also target Foxo1, and participate in the disruption of adipogenic differentiation and the regulation of insulin synthesis [63– 65]. [score:4]
Through the regulation of DLK1 level, miR-15a could disrupt adipogenic differentiation [12]. [score:2]
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[+] score: 5
In particular miR-23b, miR-199a, and miR-15a displayed increased expression during early AVC development and characterization of target genes suggests that they are involved in regulating epithelial-mesenchymal transition (EMT) signaling pathways [106]. [score:5]
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[+] score: 3
The reproducibility of these results was tested by Taqman RT-PCR, selecting 18 miRNAs (hsa-let-7a, hsa-miR-141, hsa-miR-143, hsa-miR-145, hsa-miR-17, hsa-miR-182, hsa-miR-191, hsa-miR-199a-5p, hsa-miR-200a, hsa-miR-200b, hsa-miR-222, hsa-miR-29b, hsa-miR-34a, hsa-miR-424, hsa-miR-15a, hsa-miR-199a-3p, hsa-miR-26b, hsa-miR-361-3p) previously showing at least a three-fold modulation in expression in a wide panel of PDAC cell lines 49. [score:3]
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[+] score: 3
Typically, tyrosine-protein kinase receptor (CTK-1) can be targeted by three miRNAs, including gga-miR-15c-5p, gga-miR-15a and gga-miR-16-5p. [score:3]
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[+] score: 3
CCNE1 is the target gene of miR-15/16 in human lung cancer (Bandi and Vassella 2011) and glioblastoma (Xia et al. 2009) during tumorigenesis (http://www. [score:3]
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[+] 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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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Similarly, it was shown that the deletion of the 13q14 region, which encodes both, lincRNA DLEU2 and its resident miRNA cluster hsa-mir-15a/16-1, led to chronic lymphocytic leukemia in both human [46] and mouse [47]. [score:1]
In some cases the designated lincRNAs have been found to be the primary transcripts and not actual lincRNA genes, for example MIR155HG (also known as BIC) and DLEU2 (deleted in lymphocytic leukemia 2 (non-protein coding), previously known as LEU2, are primary transcripts of their resident miRNA genes hsa-mir-155 and hsa-mir-15a/16-1, respectively. [score:1]
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[+] score: 1
In Xenopus, miR-15/17 is necessary to sharpen the Nodal gradient [57, 58]. [score:1]
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[+] score: 1
In addition, the lncRNA DLEU2 is well conserved across the vertebrates, it is a host gene for two miRNA genes, miR-15 and miR-16, both of which are also well conserved across the vertebrates (see Fig. B in S1). [score:1]
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