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21 publications mentioning gga-mir-26a

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-26a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 279
Other miRNAs from this paper: gga-mir-223, gga-mir-146a, gga-mir-126, gga-mir-451
However, with the potential for directly targeting chicken IL-2, the downregulation of miR-26a in these tumor cells could relieve the inhibitory effect on IL-2 expression assisting in the proliferative features of the transformed lymphocyte lines. [score:11]
For further evidence to show that IL-2 levels are regulated by miR-26a, we performed experiment in which the miR-26a levels in DF-1 cells are either upregulated by overexpression or downregulated by specific silencing. [score:10]
We present the data suggesting that chicken IL-2 is a direct target of miR-26a, and its downregulation could affect IL-2 expression and signalling pathways in these transformed cells. [score:9]
Western blot analysis of the IL-2 expression levels with anti-HA antibody in DF-1 cells transfected with the Wt or the mu IL-2 expression constructs showed that the IL-2 levels in constructs expressing the Wt 3' UTR was reduced by more than 20% compared to the Mu constructs (Fig 3), showing a direct silencing of IL-2 expression by miR-26a. [score:9]
Loss of expression of miR-26a also occurs in some of the human tumours such as thyroid anaplastic carcinoma [6] and Burkitt's lymphoma [9] reiterating the role of miR-26a as a tumour suppressor, the expression of which can protect from the disease progression in cancer mo dels [5, 27]. [score:9]
Suppression of miR-26a has been demonstrated in a variety of human cancers also [4- 6] suggesting that miR-26a has potential tumour suppression functions, and its downregulation could be essential for transformation. [score:8]
Some of the previous studies have shown the role of oncogenes such as c- myc in regulating miR-26a expression [4, 30, 31] and the altered expression of miR-26a in HP45 could be related to the increased c- myc expression. [score:8]
The downregulation of miR-26a can relieve the suppressive effect of this miRNA on IL-2 expression. [score:8]
Global miRNA expression profiles of a number of virus-transformed avian lymphoma cell lines have shown downregulation of gga-miR-26a expression, irrespective of molecular mechanisms of transformation or the viral aetiology. [score:8]
Our study suggests that the suppression of miR-26a could potentially relieve the inhibitory effect on IL-2 expression and could contribute to the proliferative features of the transformed lymphocyte lines. [score:7]
The expression levels of gga-miR-26a in chicken lymphoma cells transformed by 3 distinct avian oncogenic viruses, viz Marek's disease virus (MDV), avian leukosis virus (ALV) and Reticuloendotheliosis virus (REV) were consistently downregulated compared to the levels in the normal lymphocytes. [score:7]
Although miR-26a has not been implicated in the regulation of IL-2, we examined whether miR-26a downregulation in MDV-transformed chicken lymphoma cell lines do affect IL-2 expression. [score:7]
While some of the miRNAs are oncogenic, miRNAs such as miR-26a are consistently downregulated in a number of cancers, demonstrating their potential tumor suppressor functions. [score:6]
In addition to its role as a global tumor suppressor miRNA, we also provide data to show that chicken IL-2 is a direct target for miR-26a. [score:6]
This notion is supported from the roles of miR-26a in p53 tumour suppressor network [7], as well as in the regulation of transformation-related targets such as cyclin D2, SMAD1, EZH2 and PTEN [8, 9]. [score:6]
Downregulation of IL-2 expression by miR-26a. [score:6]
We show that miR-26a is globally downregulated in a number of avian lymphoma cells irrespective of the mechanisms of transformation, reiterating the highly conserved tumor suppressor function of this miRNA. [score:6]
Here, we show that such downregulation of miR-26a occur in lymphoid cell lines transformed by ALV and REV also, suggesting that miR-26a -mediated modulation of gene expression is probably crucial for lymphocyte transformation, irrespective of the viral etiology. [score:6]
Our study shows that the downregulation of miR-26a is another global pathway for the increased IL-2 expression in the lymphoma cell lines transformed by the avian oncogenic viruses MDV, ALV and REV. [score:6]
Comparative miRNA expression profiles of 7 MDV-transformed T-cell lines showed that host-encoded miRNAs such as miR-26a, miR-223, miR-150, miR-451 and miR-126 were consistently downregulated [3]. [score:6]
This downregulation of miR-26a regardless of the viral etiology and molecular mechanisms of transformation was consistent with the tumor suppressor role of this miRNA. [score:6]
For the expression of miR-26a, DF-1 cells (0.5 × 10 [6 ]in each well) of 6-well plate were transfected with 2 μg of the expression constructs. [score:5]
For overexpression, we transfected DF-1 cells with the miR-26a expression construct pEF6-miR-26a (+). [score:5]
We also examined how the changes in the expression of miR-26a affected the IL-2 expression. [score:5]
In this study we demonstrate that, in addition to its potential role as a tumour suppressor, miR-26a also functions as a modulator of IL-2 expression. [score:5]
Our study does not examine the molecular mechanisms of downregulation of miR-26a. [score:4]
We have previously demonstrated that miR-26a is downregulated in seven independently-derived MDV-transformed lymphoblastoid T cell lines [3]. [score:4]
Figure 1 Downregulation of gga-miR-26a in transformed cell lines. [score:4]
For downregulation of miR-26a, anti-miR-26a construct was transfected into DF-1 cells. [score:4]
In summary, we show that miR-26a is globally downregulated in a number of avian lymphoma cells transformed by different oncogenic viruses that use multiple pathways for inducing transformation. [score:4]
Transformed chicken cell lines show downregulation of miR-26a. [score:4]
For further validation of targeting of chicken IL-2 by miR-26a, we constructed reporter vectors with wildtype (wt) or a mutant 3' UTR sequence of the chicken IL-2 with three base-pair mutations in the predicted miRNA binding seed region (Mu) fused to the Renilla luciferase gene in psiCHECK-2 vector (Fig. 2a). [score:4]
One of the miRNAs that was consistently downregulated in a number of MDV-transformed chicken lymphoid cell lines is gga-miR-26a [3]. [score:4]
Figure 4 Regulation of chicken IL-2 expression by miR-26a in DF-1 cells. [score:4]
The identification of some of the validated targets of miR-26a including EZH2 [9], SMAD1 [26], PTEN [8] provides intriguing link to the oncogenic pathways. [score:3]
The microarray readouts of miRNA expression confirmed that the miR-26a levels in all of these cell lines were lower than the levels in normal splenocytes, although the levels of reduction varied between cell lines (Fig. 1a). [score:3]
Levels of miR-26a affect IL-2 expression. [score:3]
Construction of miR-26a expression vectors. [score:3]
Presence of a putative MEQ -binding sequence ACACA at -650 nucleotide position would suggest a role of MEQ in modulating the miR-26a expression, although further studies are required validate this. [score:3]
Reduced expression of miR-26a in MDV (MSB-1, T226S, T265L and T273S), ALV (HP45) and REV (AVOL1 and AVOL2)-transformed cell lines. [score:3]
To gain insights into the biological functions of miR-26a, we carried out bioinformatic analysis to identify potential targets of miR-26a by scanning the chicken 3' UTR sequences using the miRanda http://www. [score:3]
For silencing miR-26a expression, 5 nM of anti-gga-miR-26a or Cy-3 -labelled control anti-miRNA were transfected into DF-1, and analysed by Northern blot 48 hours later. [score:3]
For functional analysis of miR-26a -mediated silencing, IL-2 (500 ng) and miR-26a (2 μg) expression vectors were co -transfected into DF-1 cells. [score:3]
Northern blot analysis of DF-1 cells transfected with the two vectors showed that the miR-26a expression level of pEF6-miR-26a (+) transfected cells was higher than that of normal DF-1 cells or the cells transfected with the pEF6-miR-26a (-) vector (Fig. 4a). [score:3]
Figure 2 Chicken IL-2 is a target for miR-26a. [score:3]
In addition, DF-1 cells co -transfected with 5 nM each of anti-gga-miR-26a or Cy-3 labelled control anti-miRNA (Ambion) with miR-26a expression or control vectors were also used in these studies. [score:3]
Further validation of the reduced expression of miR-26a in these transformed cells was demonstrated by Northern blotting analysis on RNA extracted from these cell lines together with normal CD4+, CD4- and unsorted splenocytes (Fig 1b). [score:3]
This analysis predicted that the 3' UTR of chicken IL-2 contained a binding site for miR-26a showing its potential as miR-26a target (Fig. 2a). [score:3]
org for potential targets of miR-26a. [score:3]
As we did not have an antibody that specifically detected the chicken IL-2, we constructed vectors that expressed HA tagged-chicken IL-2 with either the wildtype 3' UTR sequence or with miR-26a binding site mutant sequence. [score:3]
Similarly, the reduced expression of miR-26a in AVOL1 and AVOL2 cell lines may also be mediated by the v- rel. [score:3]
MiR-26a expression vector and control vector were respectively co -transfected with pcDNA-IL-2-3HA-3'UTR into DF-1, and then cells were examined by western blot analysis (Fig. 4c). [score:2]
For the construction of gga-miR-26a expression plasmids, the miR-26a primary gene together with ~200-bp flanking sequences were amplified from chicken genomic DNA using primer pairs (5'-ATGTTCTTTAATGTCGGGAGC-3') and (5'-AAAGAATTCTGCCCGTGAC-3'), and cloned into pEF6-V5/His TOPO vector (Invitrogen) under control of EF1α promoter vector. [score:2]
Targeting of chicken IL-2 by miR-26a in reporter assays. [score:2]
It showed that the IL-2 expression level was reduced by more than 30% in the presence of miR-26a compared to the levels in cells transfected with pEF6-miR-26a (-) control vector. [score:2]
In contrast, the IL-2 expression level was increased by more than 140% when the miR-26a levels were silenced using the anti-miR-26a compared to the anti-miRNA control (Fig. 4d). [score:2]
As the negative control, we used the construct pEF6-miR-26a (-), in which the miRNA was cloned in the reverse orientation. [score:1]
In contrast, the signals of miR-26a were very low in all transformed cell lines, including those transformed by ALV and REV. [score:1]
In some MD lymphoma lines (T226S, T265L & T273S), the miR-26a levels were undetectable. [score:1]
DNA oligonucleotide with the complementary sequence to miR-26a was end labelled with [γ- [32]P] ATP by T4 polynucleotide kinase (New England Biolabs). [score:1]
The levels of miR-26a signal detected were very high in normal splenocytes, with no major differences between CD4+ and CD4- T cell populations. [score:1]
We have now extended the analysis to examine the levels of miR-26a in four of the above MDV-transformed cell lines together with ALV-transformed cell line HP45 and REV-transformed cell lines AVOL1 and AVOL2. [score:1]
Reporter assays on DF-1 cells that express endogenous miR-26a demonstrated that the luciferase reporter levels in the cells transfected with the Wt-3' UTR reporter construct was reduced by nearly 35% (p < 0.05) compared to the Mu-3' UTR construct (Fig. 2b). [score:1]
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2
[+] score: 80
Their study showed that several host-encoded miRNAs, including gga-miR-155, gga-miR-150, gga-miR-451, gga-miR-26a, and gga-miR-223, were down-regulated in all MDV-transformed cell lines compared to normal splenocytes, and nine MDV-1-encoded miRNAs were up-regulated in all of the MDV-transformed cell lines compared to the MDV -negative reticuloendotheliosis virus (REV)-T-transformed cell line AVOL-1. Previous studies have mainly focused on miRNA profiles of MDV-infected CEF and MDV-transformed cell lines and expression of several individual miRNAs in MDV -induced splenic tumors. [score:7]
EIF3A, another predicted target gene of miR-26a was up-regulated in tumorous spleen of our previous study [33]. [score:6]
Six miRNAs (gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-222, gga-miR-199*, and gga-miR-140*) were down-regulated and one miRNA (miR-146c) was up-regulated in MDV-infected samples, and especially in MD lymphomas, compared to non-infected samples. [score:6]
Chen et al. showed that miR-26a inhibited cell growth and colony formation, induced a G1 arrest in NPC cells, and suppressed tumorigenesis in a murine mo del of NPC xenograft [53]. [score:5]
Putative target genes of gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-222, gga-miR-155, gga-miR-146b, and gga-miR-146c were predicted by TargetScan (Version 6.0) [31]. [score:5]
Significant interaction of miR-26a and EIF3A was verified in the current study by using the luciferase reporter gene assay, which indicated that down-regulation of miR-26a could induce expression of EIF3A in MD lymphoma. [score:5]
In addition, miR-26a was also down-regulated in seven independently-derived MDV-transformed lymphoblastoid T cell lines, and ALV and REV transformed lymphoid cell lines [21]. [score:4]
gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-199*, and gga-miR-140* were down-regulated (Figure 2A–E). [score:4]
Suppression of miR-26a has been demonstrated in various human cancers, such as thyroid anaplastic carcinoma [50] and Burkitt’s lymphoma [34], [50]– [52]. [score:3]
In the current study, miR-181a and miR-26a were down-regulated in tumorous spleen and MD lymphoma, compared to non-infected spleen. [score:3]
As the only known target gene of miR-26a, EZH2, acting as an oncogene, was shown to be involved in proliferation of different cell types, including tumor cell lines [54]; it showed oncogenic activity and tumor transformation requiring histone methylatransferase activity. [score:3]
The gga-miR-26a mimic inhibited luciferase activity of pmiR-RB-REPORT-EIF3A UTR by 24% (Figure 5C). [score:3]
Additionally, because of previous reports on gga-miR-26a [18], [21], [23], it was also chosen to be verified by qPCR, which showed down-regulation in MD lymphoma from liver compared with non-infected lymphocytes and non-infected spleen in the current study (Table S9). [score:3]
Some host miRNAs, including gga-miR-let-7, gga-miR-199a-1, gga-miR-26a, gga-miR-181a, and gga-miR-16, were expressed at lower levels in MDV -induced tumors than non-infected spleens, indicating their potential importance in tumorigenesis. [score:3]
Only one target gene for miR-26a, EZH2 was reported previously [34]. [score:3]
B. Expression of gga-miR-26a among TS, LL, and NS. [score:3]
A recent miRNA microarray study has shown that miR-26a was down-regulated in nasopharyngeal carcinoma (NPC) tissues compared with adjacent normal tissues [53]. [score:3]
To further verify the interaction of predicted target genes and miRNAs, we conducted luciferase reporter gene assays to detect interaction of gga-miR-181a with MYBL1 and IGF2BP3, gga-miR-26a with EIF3A, and gga-miR-221 with BCL11B. [score:2]
miR-26a is considered to be a potential tumor suppressor [49]. [score:2]
Interactions of miRNAs and predicted target genes, including gga-miR-181a with MYBL1 and IGF2BP3, and gga-miR-26a with EIF3A, were discovered by using the luciferase reporter gene assay. [score:2]
These results demonstrate significant interaction of gga-miR-181a with MYBL1 and IGF2BP3, and of gga-miR-26a with EIF3A. [score:1]
The gga-miR-181a mimic, gga-miR-26a mimic, gga-miR-221 mimic and their corresponding negative controls (Ribobio Co. ) [score:1]
C. Interaction validation for gga-miR-26a and EIF3A. [score:1]
0051003.g004 Figure 4 A. Schema of binding site for gga-miR-181a and MYBL1; B. Schema of binding site for gga-miR-181a and IGF2BP3; C. Schema of binding site for gga-miR-26a and EIF3A; D. Schema of binding site for gga-miR-221 and BCL11B. [score:1]
A. Schema of binding site for gga-miR-181a and MYBL1; B. Schema of binding site for gga-miR-181a and IGF2BP3; C. Schema of binding site for gga-miR-26a and EIF3A; D. Schema of binding site for gga-miR-221 and BCL11B. [score:1]
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3
[+] score: 72
The expression patterns of gga-miR-1a and gga-miR-21 were similar in the different developmental stages; relatively lower expression was observed from 42-d to 110-d compared with 162-d and increased dramatically to peak in 162-d. However, the expression dynamics of gga-miR-26a were different; the highest expression level was found in the 42-d ovary, then decreased from 70-d to 110-d, and finally increased in the 162-d ovary although still lower than 42-d. The expression of gga-miR-137 and gga-miR-375 in ovary decreased significantly from 42-d to 162-d. Figure 4 Expression patterns of gga-miR-1a, gga-miR-21, gga-miR-26a, gga-miR-137 and gga-miR-375 in different developmental stages of ovary and in different sized follicle in chicken by qRT-PCR assays. [score:13]
The expression patterns of gga-miR-1a and gga-miR-21 were similar in the different developmental stages; relatively lower expression was observed from 42-d to 110-d compared with 162-d and increased dramatically to peak in 162-d. However, the expression dynamics of gga-miR-26a were different; the highest expression level was found in the 42-d ovary, then decreased from 70-d to 110-d, and finally increased in the 162-d ovary although still lower than 42-d. The expression of gga-miR-137 and gga-miR-375 in ovary decreased significantly from 42-d to 162-d. Figure 4 Expression patterns of gga-miR-1a, gga-miR-21, gga-miR-26a, gga-miR-137 and gga-miR-375 in different developmental stages of ovary and in different sized follicle in chicken by qRT-PCR assays. [score:13]
It has also been reported that miR-30c, let-7a, let-7b and let-7c were up-regulated, while miR-30d, miR-29a and miR-26a were down-regulated in rat granulosa cells treated with FSH for 12 h, which suggests that these miRNAs participate in FSH -mediated progesterone biosynthesis of granulosa cells [45]. [score:7]
One study showed that, during myogenesis, overexpression of miR-26a targets the enhancer of Zeste homolog 2 (Ezh2), which normally suppresses skeletal muscle differentiation [52]. [score:7]
In this study, gga-let-7b is up-regulated while gga-let-7 g, gga-miR-17-3p gga-miR-30d, gga-miR-29a, gga-miR-26a and gga-miR-181a are all down-regulated in the mature ovary compared with the immature ovary. [score:6]
To validate the Illumina small RNA deep sequencing data, five differentially expressed miRNAs (gga-miR-1a, gga-miR-21, gga-miR-26a, gga-miR-137 and gga-miR-375) were selected, and their expression levels were quantified using real-time quantitative RT-PCR (qRT-PCR). [score:5]
In MCF7 cancer cells, estradiol can repress miR-26a expression to regulate numerous genes associated with cell growth and proliferation [44]. [score:4]
The expression of gga-miR-375 was relatively lower in LW and SF follicles, increased most in the F6-F2 follicles and then declined in the F1 stage, suggesting an important role of gga-miR-26a and gga-miR-137 in hierarchy maintenance of follicles in chicken. [score:3]
For gga-miR-26a and gga-miR-137, the highest expression level was found in the SF (6–8 mm) follicle. [score:3]
To further characterize the functionality of these differentially expressed miRNAs identified from the chicken ovary, the expression levels of gga-miR-1a, gga-miR-21, gga-miR-26a, gga-miR-137 and gga-miR-375 were further examined in ovary tissues from 42-, 70-, 90-, 110- and 162-day-old White Leghorn hens (n =3), as well as in follicles isolated from ovaries of 162-day-old White Leghorn hens, namely, a large white follicle (LW, diameter =2-4 mm), small yellow follicle (SF, diameter =6-8 mm), F6 (diameter =12-14 mm), F4 (diameter =22-24 mm), F2 (diameter =30-31 mm) and F1 (diameter =34 mm) follicles. [score:3]
miR-26a was also found to play a role in normal tissue growth and development and to have an impact on cell proliferation and differentiation. [score:2]
In osteogenesis, miR-26a was found to regulate osteoblast cell growth and differentiation in human adipose tissue-derived stem cells [53]. [score:2]
miR-26a is reported to have anti-apoptotic effects in many cancers [48- 51]. [score:1]
SF were to be chosen from pre-hierarchical follicles (<8 mm) to pre-ovulatory hierarchy follicles (>10 mm), therefore, gga-miR-26a is likely associated with the mechanism of recruitment of dominant follicle in chicken. [score:1]
Furthermore, gga-miR-101, gga-miR-1a, gga-miR-146c, gga-miR-148a, gga-miR-126, gga-miR-26a and gga-miR-30d were abundant in our sequencing libraries, as has been shown in other animal gonads [25, 27, 28]. [score:1]
In this study, the highest level of gga-miR-26a was found in SF follicles. [score:1]
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4
[+] score: 23
For example, miR-26a is globally down-regulated in a number of avian lymphoma cells, reiterating the highly conserved tumor suppressor function of this miRNA. [score:6]
One established function of IL-2 is in the regulation of T-cell proliferation, which suggests that the decreased expression in miR-26a and the subsequent increase in IL-2 expression could be a conserved mechanism in avian viral transformation. [score:6]
The host miRNAs downregulated in the MDV-transformed cell lines include miR-155, miR-223, miR-150, miR-451, and miR-26a. [score:4]
Functional analysis revealed that miR-26a regulates the expression of interleukin 2 (IL-2) [46]. [score:4]
Xu H. Yao Y. Smith L. P. Nair V. MicroRNA-26a -mediated regulation of interleukin-2 expression in transformed avian lymphocyte lines Cancer Cell Int. [score:3]
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5
[+] score: 20
Interleukin-2 (IL-2) is essential for the growth and proliferation of T-cells (Cantrell and Smith, 1984), and we have previously shown the downregulation of miR-26a in MDV-transformed cell lines, where the decreased expression relieved its suppressive effect on the interleukin-2, potentially allowing proliferation (Xu et al., 2010). [score:8]
Expression levels of miRNAs obtained from the deep sequencing data were validated by carrying out quantitative RT-PCR on gga-miR-21, gga-miR-26a, gga-miR-142-3p and gga-miR-155 using RNA extracted from different cell types. [score:3]
This included gga-miR-26a which showed a 4.5-fold decrease in expression. [score:3]
MicroRNA-26a -mediated regulation of interleukin-2 expression in transformed avian lymphocyte lines. [score:3]
Validation of expression levels of gga-miR-21, gga-miR-26a, gga-miR142-3p, gga-miR-155 and gga-miR-223 was carried out by quantitative RT-PCR using procedures described (Yao et al., 2008). [score:3]
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6
[+] score: 16
Among the miRNAs quantified here, miR-30d and miR-26a were down-regulated in F2 birds with higher AbF content, and these results were confirmed by qPCR in the birds with phenotypic extremes of AbF. [score:4]
Previous work demonstrated that miR-30d and miR26a are highly expressed in chicken preadipocytes 19 and that miR-30d influences the transcription of insulin 25. [score:3]
Eleven of these (miR-204, miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-122-5p, miR-103-3p, miR-27b-3p, miR-92-3p, miR-142-3p, and miR-17-5p) have been implicated, directly or indirectly, in fat deposition; 9 showed a high fold-change (miR-3535, miR-144-3p, miR-30e-5p, miR-301b-3p, miR-215-5p, miR-200a-3p, miR-133a-3p, miR-133c-3p, and miR-146b-5p). [score:3]
Taken together, these findings indicate that miR-30d and miR-26a are likely to play important regulatory roles in lipid mechanism in chickens. [score:2]
Specifically, the integrated analysis of DEMs and DEGs suggests that nine miRNAs (gga-miR-19a-3p, miR-19b-3p, miR-17-5p, miR-30d, miR-26a, miR-103-3p, miR-27b-3p, miR-142-3p, and miR-92-3p) and three genes (ACSL1, FADS2 and ABCD3) are strong candidate miRNAs and genes involved in regulating the accumulation of AbF in chickens. [score:2]
Some of the DEMs identified by deep sequencing (miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-30a-5p, miR-122-5p, miR-103, miR-125b, and miR-17-5p) are known to influence mammalian lipid metabolism. [score:1]
However, many important candidate miRNAs related to lipid mechanism (e. g., gga-miR-301b-3p, gga-miR-130b-3p, gga-miR-30a-5p, gga-miR-142, gga-miR-146b, gga-miR-103, gga -miR-26a, etc. ) [score:1]
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7
[+] score: 16
gga-miR-221/222 suppresses the cell cycle of T-cell lymphoma in Marek's disease (MD) (Lambeth et al., 2009), and gga-miR-181a and gga-miR-26a inhibit proliferation of Marek's disease lymphoma cells (Li X. et al., 2014; Lian et al., 2015). [score:9]
gga-miR-26a targets NEK6 and suppresses Marek's disease lymphoma cell proliferation. [score:7]
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8
[+] score: 11
For example, miR-520b suppressed tumour formation in breast cancer and hepatocellular carcinoma by targeting MAP3K2 and cyclin D1, miR17/20a inhibited tumour growth via targeting the MAP3K2-Erk5 pathway in vivo [43], and miR-26a promoted glioblastoma cell growth in vitro via targeting MAP3K2 [30]. [score:11]
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9
[+] score: 8
Two other miRNAs, gga-miR-26a and gga-miR-181a, were highly expressed and ranked as the third and fourth most highly expressed miRNAs, respectively. [score:5]
Leeper et al. also demonstrated that miR-26a could inhibit cellular differentiation and apoptosis by altering the TGFβ signaling pathway [34]. [score:3]
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10
[+] score: 8
Of the top 20 abundantly expressed miRNAs identified, some, such as miR-133, miR-10b, miR-26a, miR-30e and gga-miR-30a were also abundantly expressed in chicken somites [41]. [score:5]
miRNAs Normalized Reads Total Reads WRRh WRRl XHh XHl gga-miR-133a 3,558,683 3,069,071 1,997,286 2,607,787 11,232,827 gga-miR-133c 3,350,936 2,885,440 1,878,925 2,449,209 10,564,510 gga-miR-133b 3,326,848 2,864,578 1,864,721 2,431,274 10,487,421 gga-let-7a 1,699,621 1,513,865 857,210 1,133,532 5,204,228 gga-miR-22-3p 1,333,233 1,145,421 712,464 988,186 4,179,304 gga-miR-30a-5p 1,213,468 1,148,128 790,893 930,507 4,082,996 gga-miR-26a 1,212,635 1,054,689 691,456 1,006,522 3,965,302 gga-miR-30d 851,887 813,262 583,932 667,002 2,916,083 gga-miR-181a-6p 918,452 836,452 485,661 650,836 2,891,401 gga-miR-10a-5p 943,686 782,180 420,809 663,401 2,810,076 gga-miR-10b 911,725 757,564 398,852 633,567 2,701,708 gga-miR-30e 799,679 730,832 501,718 596,218 2,628,447 gga-let-7j 848,972 756,205 428,182 566,165 2,599,524 gga-let-7f 398,292 363,598 206,995 274,333 1,243,218 gga-miR-148a 288,585 300,432 144,015 180,973 914,005 gga-miR-146c-5p 224,147 207,782 171,443 132,712 736,084 gga-let-7k 211,853 206,518 118,297 155,412 692,080 gga-let-7c 242,661 189,820 111,118 139,257 682,856 gga-miR-199-3p 168,417 152,158 75,346 121,460 517,381 gga-miR-126-5p 139,914 109,805 89,607 86,681 426,007 Differentially expressed miRNAs were identified by DEGseq analysis (fold change > 1.5 or < 0.66; p-value < 0.05; q-value < 0.01), as a result, 200, 279, 257 and 297 miRNAs were detected in four comparisons of WRRh vs. [score:3]
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11
[+] score: 7
Other miRNAs from this paper: gga-mir-101-1, gga-mir-21, gga-mir-101-2
Li X. Lian L. Zhang D. Qu L. Yang N. gga-miR-26a targets NEK6 and suppresses Marek’s disease lymphoma cell proliferation Poult. [score:7]
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In known miRNAs, gga-miR-26a-5p displayed greater than 12 M reads and exhibited the highest expression level followed by gga-miR-99a-5p, which displayed greater than 5 M reads. [score:3]
miR-26a regulates tissue and cell growth and differentiation [61, 62] and has anti-apoptotic effects on many cancers [63– 65]. [score:2]
In pituitary and hypothalamic libraries, gga-miR-26a-5p (>12 M reads) and gga-miR-99a-5p (>5 M reads) were the most two frequently sequenced miRNAs. [score:1]
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gga-mir-26a inhibited IL-2 mRNA and was decreased in seven MD transformed cell lines [89, 90], but again in our dataset, neither gga-mir-26a nor IL-2 were differentially expressed and neither was IL-2 protein. [score:5]
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In addition, the similar phenomenon was also observed in S. mansoni (miR-4, miR-6, miR-9, miR-32, miR-125, miR-3, and miR-5 were expressed in adult worms only, and miR-20, miR-18, miR-22, miR-26, and bantam were expressed in schistosomula only) (Simoes et al., 2011). [score:5]
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Gene targeted by the disease miRNA26. [score:5]
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The top five highly expressed miRNAs were gga-miR-215-5p, gga-miR-10b-5p, gga-miR-21-5p, gga-miR-26-5p, and gga-miR-22-3p, accounting for 40.54, 7.76, 6.78, 6.43, and 6.35% of total known miRNA reads, respectively. [score:3]
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Ten mature miRNAs with the highest expression comprised approximately 50% of all miRNAs, showing a relatively abundant distribution (Fig.   5D), while miR-21, miR-26a, miR-125b, miR-101, and miR-199 were the most abundant miRNAs overall, together accounting for 33% of the total. [score:3]
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Other miRNAs from this paper: gga-mir-155, gga-mir-26a-2
Due to involvement in these pathways, it comes as no surprise that the CTDSP1/2/L and the miR-26 family have been implicated in tumorigenesis. [score:1]
Further, CTDSP1/2/L genes have all been found to contain an intronic microRNA that belongs to the miR-26 family. [score:1]
For instance, CTDSP1/2/L genes have an intronic microRNA from the miR-26 family. [score:1]
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Figure 2 The muscle specific miRNAs (myo-miR), miR-133a/b, miR-206, miR-486, miR-26a, miR-27b, miR-378, miR-148a and miR-181 were highly enriched in skeletal muscle and play key roles in skeletal muscle metabolism [11]. [score:1]
The novel miRNAs 7_32745, 17_11642, 7_32911 and 15_10888 were homologous with miR-10a-5p, miR-181a-5p, miR-26-5p and miR-130a-3p respectively (Supplementary Table 2). [score:1]
Figure 2The muscle specific miRNAs (myo-miR), miR-133a/b, miR-206, miR-486, miR-26a, miR-27b, miR-378, miR-148a and miR-181 were highly enriched in skeletal muscle and play key roles in skeletal muscle metabolism [11]. [score:1]
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Regulation signature of miR-143 and miR-26 in porcine Salmonella infection identified by binding site enrichment analysis. [score:2]
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In addition, some other miRNAs, such as miR-148a, miR-122, miR-21-5p, Let-7f-5p, miR-26a-5p, miR-126-5p, miR-30d, and miR-10a-5p, were also highly abundant in chicken liver. [score:1]
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