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13 publications mentioning gga-mir-23b

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-23b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 175
Other miRNAs from this paper: gga-mir-19a, gga-mir-18a, gga-mir-200b, gga-mir-383
Acting as an oncogene, miR-23b expression is up-regulated in glioma, and miR-23b down-regulation could suppress glioma cell growth and invasion by targeting the VHL gene 40. [score:13]
During ALV-J invasion, miR-23b up-regulation could decrease the expression of IRF1 and further down-regulate the expression of IFNβ. [score:11]
In human cervical cancer, the oncogenic HPV-16 E6 protein reduces the expression of miR-23b, which subsequently increases the expression of its target uPA, and this increased expression may contribute to the migration of human cervical cancer cells 26. [score:9]
In summary, our study presented evidence that the expression of miR-23b was up-regulated in ALV-J-infected chicken spleens and that IRF1 is a target of miR-23b. [score:8]
In the current study, IRF1 was predicted to be a potential miR-23b target by the miRNA-target interaction network, and opposing expression patterns for miR-23b and IRF1 were identified. [score:7]
Through Solexa deep sequencing, we found that miR-23b was up-regulated in ALV-J-infected spleens compared to uninfected spleens, while its target gene IRF1 had an opposing expression pattern. [score:7]
Moreover, with anti-miR-23b treatment, the expression of IFNβ was sharply up-regulated (P = 0.0004). [score:6]
Interestingly, our analysis showed that miR-23b and its putative target IRF1 had opposing expression patterns in uninfected samples and ALV-J-infected samples (Fig. 5A). [score:5]
These results suggested that miR-23b overexpression could strengthen ALV-J replication, whereas its loss of function could inhibit ALV-J replication. [score:5]
The 3′ UTR of IRF1 is directly targeted by miR-23bTo validate the target relationship between miR-23b and IRF1, a dual-luciferase reporter gene assay was conducted in DF-1 cells. [score:5]
The mRNA expression levels of IRF1 significantly decreased (P = 0.00034) when cells were transfected with a miR-23b mimic (Fig. 6C) and significantly increased (P = 0.00037) after transfection with anti-miR-23b (Fig. 6D), which confirmed that IRF1 is a target of miR-23b. [score:5]
Validation of IRF1 as a direct target of miR-23b. [score:4]
Similarly, this study found that miR-23b was up-regulated in ALV-J-infected chicken spleens. [score:4]
These results suggested that up-regulated miR-23b may be associated with ALV-J invasion and avian leukosis formation. [score:4]
miR-23b is highly conserved in most vertebrates and is up-regulated in various human cancers. [score:4]
As shown in (Fig. 5D), luciferase activity in the DF-1 cell lines significantly (P = 0.0002) decreased when a miR-23b mimic was co -transfected with pmir-GLO-IRF1-WT containing a miR-23b binding sequence, whereas luciferase activity did not significantly (P = 0.0325) change when transfected with pmir-GLO-IRF1-MT, indicating that miR-23b may directly target the chicken IRF1 3′ UTR. [score:4]
The 3′ UTR of IRF1 is directly targeted by miR-23b. [score:4]
To study the function of IRF1 and its regulator miR-23b, which is involved in ALV-J invasion, transfected HD11 cells were challenged with ALV-J, and then qPCR and Western blot were used to detect the expression levels of gp85. [score:4]
During virus invasion, miR-23b exhibits antiviral functions against rhinoviruses by down -regulating its target VLDLR, which acts as a receptor for rhinovirus infection 27. [score:4]
To construct a miR-23b target luciferase reporter (pmir-GLO-IRF1-WT), the segment sequence of the IRF1 3′ UTR (616 bp) that contained the putative miR-23b binding sequence was amplified by PCR using a cDNA template synthesized from total RNA. [score:3]
The suppression of miR-23b may reduce cancer cell migration, invasion, growth and angiogenesis in human colon cancer 39. [score:3]
Network analysis showed that IRF1 is also a target of gga-miR-23b and gga-miR-2964 (Fig. 4). [score:3]
The miR-23b mimics, mimic control duplexes, anti-miR-23b antagomirs, anti-NC, siRNA target against the IRF1 gene (si-IRF1) and siRNA nonspecific control duplex were designed and synthesized by GenePharma (GenePharma). [score:3]
To generate a miR-23b target-mutated reporter (pmir-GLO-IRF1-Mut), mutations were achieved by changing the miR-23b binding seed sequences from AATGTGA to CCGAGTG using the megaprimer PCR method. [score:3]
The qPCR results revealed that the expression patterns of miR-23b and IRF1 were consistent with the Solexa deep sequencing data. [score:3]
The opposing expression patterns of miR-23b and IRF1 in ALV-J-infected and uninfected samples were confirmed by qPCR. [score:3]
The transfection efficiency analysis showed that 50 nM and 100 nM of a miR-23b mimic could significantly (P = 0.0189) and highly significantly (P = 0.0022) decrease IRF1 expression levels in DF-1 cells at 48 h after transfection, respectively (Fig. 5B). [score:3]
The expression of ALV-J gp85 was remarkably increased in challenged HD11 cells that were transfected with a miR-23b mimic. [score:3]
The full-length blots with IRF1 overexpression, si-IRF1, miR-23b mimic and anti-miR-23b are presented in Supplementary Figure S3 A-H, respectively. [score:3]
However, the expression levels of gp85 increased after transfection with a miR-23b mimic (Fig. 6C) but decreased upon transfection with anti-miR-23b (Fig. 6D), although in both cases, the changes were not statistically significant. [score:3]
In the current study, we focused on miR-23b partly because its potential target gene IRF1 is known to exert antiviral effects. [score:3]
miR-23b plays a significant role in tumorigenesis 26 and inhibits virus infection 27. [score:3]
For miRNA expression analysis, reverse transcription was performed using a ReverTra Ace qPCR RT Kit (Toyobo) with a gga-miR-23b bulge-loop RT primer. [score:2]
To validate the target relationship between miR-23b and IRF1, a dual-luciferase reporter gene assay was conducted in DF-1 cells. [score:2]
Therefore, we hypothesized that miR-23b might be involved in controlling host immune defenses through the regulation of IRF1. [score:2]
Therefore, miRNA-target interactions between miR-23b and the IRF1 gene can be considered candidates for further study. [score:2]
The mutation sequence in the miR-23b binding site is highlighted in blue. [score:2]
When the cells grew to 80% confluence, they were transfected with (I) 1.6 μg of pcDNA3.1-IRF1; (II) 100 nM si-IRF1; (III) 100 nM miR-23b mimic and (IV) 100 nM anti-miR-23b using Lipofectamine 2000 reagent. [score:1]
After transfection with pcDNA3.1-IRF1, si-IRF1, miR-23b mimic and anti-miR-23b, HD11 cells were inoculated with 50% tissue culture infectious doses (TICD [50]) of ALV-J. 72 h later, HD11 cells were subjected to Western blot analysis as previously report 24. [score:1]
Actually, the protein levels for gp85 was either increased by 2.07-fold (Fig. 7C) or was decreased by 0.53-fold (Fig. 7D), in response to miR-23b mimic or anti-miR-23b tranfection. [score:1]
In vitro experiments show that IRF1 and miR-23b could affect ALV-J replicationThe genome of ALV-J is composed of three coding genes: gag, pol and env. [score:1]
DF-1 cells were seeded in 96-well plates one day before transfection and then co -transfected with 100 ng of IRF1 3′ UTR wild-type or mutant constructs and 100 nM of miR-23b mimics or mimic control duplexes using Lipofectamine 2000 reagent. [score:1]
Western Blot analysis of the effects of IRF1 and miR-23b on ALV-J replication. [score:1]
This finding provides novel insights into the involvement of miR-23b in ALV-J infection. [score:1]
Furthermore, the role of miR-23b as a regulatory factor of IRF1 was confirmed by the dual-luciferase reporter assay. [score:1]
Quantitative analysis of the effects of IRF1 and miR-23b on ALV-J replication. [score:1]
Several previous studies have provided evidence for the involvement of miR-23b in tumorigenesis and viral integration. [score:1]
In vitro experiments show that IRF1 and miR-23b could affect ALV-J replication. [score:1]
Transfection of pcDNA3.1-IRF1, si-IRF1, miR-23b mimics, and anti-miR-23b and preparation of ALV-J. Western Blot. [score:1]
The miR-23b mature sequence and its binding seed sequence in IRF1 are shown in (Fig. 5C). [score:1]
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2
[+] score: 13
Sequence alignments show miR predicted targets sites within the 3’UTR of chick Spry2 and chick microRNA sequences of mir-21, mir-23, mir-27, mir-122, and miR-128. [score:3]
In our hands, only mir-23, mir-27 and mir-128 showed strong expression in somites (Figure 6B). [score:3]
Our analysis of Targetscan followed by Northern blots of developing somites showed that mir-23, mir-27 and mir-128 could be part of this negative feedback loop mechanism. [score:3]
We also propose that mir-23, mir-27 and mir-128 could be part of the negative feedback loop mechanism. [score:1]
However, further analysis using gain- and loss-of-function of mir-23, mir-27 and mir-128 is required to proof or to exclude an interaction with FGF/Spry2 signalling. [score:1]
RNA was transferred to five membranes (Hybond NX, Amersham Biosciences) then hybridized to [32]P-labeled antisense probes (end -labelled with [γ- [32]P]ATP and T4 kinase) complementary to the mature mirRNA of gga-miR-21, gga-miR-23, gga-miR-27, gga-miR-122 and gga-miR-128 that cover the entire length of the miRNAs. [score:1]
The analysis showed that mir-21, mir-23, mir-27, mir-122 and mir-128 can potentially interact with Spry2 through binding to its 3’UTR (Figure 6A). [score:1]
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3
[+] score: 12
Other miRNAs from this paper: hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-30a, hsa-mir-32, hsa-mir-33a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-147a, hsa-mir-34a, hsa-mir-187, hsa-mir-204, hsa-mir-205, hsa-mir-200b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-138-2, hsa-mir-142, hsa-mir-144, hsa-mir-125b-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-190a, hsa-mir-200c, hsa-mir-155, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-365b, hsa-mir-328, gga-mir-33-1, gga-mir-125b-2, gga-mir-155, gga-mir-17, gga-mir-148a, gga-mir-138-1, gga-mir-187, gga-mir-32, gga-mir-30d, gga-mir-30b, gga-mir-30a, gga-mir-30c-2, gga-mir-190a, gga-mir-204-2, gga-mir-138-2, gga-let-7d, gga-let-7f, gga-mir-146a, gga-mir-205b, gga-mir-200a, gga-mir-200b, gga-mir-34a, gga-mir-30e, gga-mir-30c-1, gga-mir-205a, gga-mir-204-1, gga-mir-142, hsa-mir-449a, hsa-mir-489, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-33b, hsa-mir-449b, gga-mir-146b, gga-mir-147, gga-mir-489, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-144, gga-mir-460a, hsa-mir-147b, hsa-mir-190b, gga-mir-22, gga-mir-460b, gga-mir-1662, gga-mir-1684a, gga-mir-449c, gga-mir-146c, gga-mir-449b, gga-mir-2954, hsa-mir-548aa-1, hsa-mir-548aa-2, 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-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, gga-mir-365b, gga-mir-33-2, gga-mir-125b-1, gga-mir-190b, gga-mir-449d, gga-mir-205c
In this study, we found that miR-155, miR-23b-3p, miR-146b-5p and miR-146b-3p upregulated in AS broilers’ pulmonary arteries tissue. [score:4]
Considering the differential expressions of miR-155, miR-23b-3p, miR-146b-5p and miR-146b-3p found in the AS broiler pulmonary artery tissues in this study, we proposed these four miRNAs may also serve as a key regulator to pulmonary artery remo deling during AS progress. [score:4]
In addition, the pattern of differential expression for miR-23b-3p was reported to contribute to the proangiogenic response [20]. [score:3]
The predicted functions of mir-23b-3p showed significant associations with the migration of phagocytes, the proliferation of mononuclear leukocytes and the cell movement of smooth muscle cells [20]. [score:1]
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4
[+] score: 12
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-15a, 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-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
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]
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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5
[+] score: 9
We previously showed that miRNA-23b promotes ALV-J replication by targeting interferon regulatory factor-1 (IRF1; Li et al., 2015). [score:4]
To date, several miRNAs, including gga-miR-221, gga-miR-222, gga-miR-23b, gga-miR-375, gga-miR-125b, gga-miR-1650, gga-miR-193a, gga-miR-193b, gga-let-7b, gga-let-7i, gga-miR-458, gga-miR-1456, gga-miR-1704, gga-miR-1777, gga-miR-1790, and gga-miR-2127, have been reported to be associated with tumorigenesis and the aberrant expression of the retrovirus, ALV-J (Li et al., 2012; Wang et al., 2013a, b; Li H. et al., 2014; Dai et al., 2015; Li et al., 2015). [score:3]
MicroRNA-23b promotes avian leukosis virus subgroup J (ALV-J) replication by targeting IRF1. [score:2]
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6
[+] score: 8
During ALV-J infection, miR-23b targeted IRF1 and down-regulated IFN-β expression, further promoting ALV-J replication (21). [score:8]
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7
[+] score: 7
Our previous study demonstrated that IRF1 expression was decreased as a target of miR-23b in the White (Recessive) Plymouth Rock chickens with ALV-J infection (Li et al., 2015). [score:5]
MicroRNA-23b Promotes Avian Leukosis Subgroup J (ALV-J) Replication by Targeting IRF1. [score:2]
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8
[+] score: 6
Wang et al. identified 32 known miRNAs from skeletal muscle of Arbor Acres commercial chickens, of which 12 form five clusters: miR-133a-1-miR-1a-2, miR-23b-miR-24, miR-99a-let-7c, miR-92-miR-19b-miR-18a-miR-17, and miR-30e-miR-30c-1, suggesting that most miRNAs co-express in skeletal muscle [85]. [score:3]
3.4Wang et al. identified 32 known miRNAs from skeletal muscle of Arbor Acres commercial chickens, of which 12 form five clusters: miR-133a-1-miR-1a-2, miR-23b-miR-24, miR-99a-let-7c, miR-92-miR-19b-miR-18a-miR-17, and miR-30e-miR-30c-1, suggesting that most miRNAs co-express in skeletal muscle [85]. [score:3]
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9
[+] score: 6
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]
Bonet F. Duenas A. Lopez-Sanchez C. Garcia-Martinez V. Aranega A. E. Franco D. Mir-23b and mir-199a impair epithelial-to-mesenchymal transition during atrioventricular endocardial cushion formation Dev. [score:1]
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10
[+] score: 5
In this study, FADS1 was targeted by miR-365-3p, miR-218-5p, miR-181a-5p, miR-181b-5p, miR-29a-3p, and miR-23b-3p, whereas FADS2 was targeted by miR-30c-1-3p. [score:5]
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11
[+] score: 3
Other chicken miRNAs that are expressed at high levels in IAH30 cells include gga-miR-24 (5.5%), gga-miR-27b (4%), gga-miR-19b (3.9%), gga-miR-20a (3.9%), gga-miR-148a (3.7%), gga-miR-23b (3%), and gga-miR-92 (3%). [score:3]
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12
[+] score: 3
Analysis also showed that the enrichment of the targets of other miRNAs such as gga-miR-9*, gga-miR-217, gga-miR-19a and gga-miR-23b was also significant. [score:3]
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13
[+] score: 2
Other miRNAs from this paper: gga-mir-7-1, gga-mir-27b, gga-mir-142, gga-mir-1456, gga-mir-7439
The color of the edge indicates the type of epistatic effect (AA = red; AD = purple; DA = blue; DD = green) Table 3 The SNPs on GGAZ interacted with the SNPs on GGA21, and the Refgenes in the two important regions Chr Position Locus RS# Refgenes Z37,246,32137,440,77037,562,58238,066,34638,424,44838,545,04438,795,33939,120,19839,189,94639,223,66839,256,77039,415,37840,393,05840,411,58540,514,08541,304,56145,300,03045,695,92746,745,968Gga_rs14765324Gga_rs16768474Gga_rs14765605Gga_rs16768723Gga_rs14766107GGaluGA351567Gga_rs16047676Gga_rs16781643Gga_rs14745723Gga_rs16131986Gga_rs14787078Gga_rs16781713Gga_rs14787751Gga_rs16782083Gga_rs16754179Gga_rs16132921Gga_rs14015526GGaluGA352176Gga_rs14016510rs14765324rs16768474rs14765605rs16768723rs14766107rs317567123rs16047676rs16781643rs14745723rs16131986rs14787078rs16781713rs14787751rs16782083rs16754179rs16132921rs14015526rs316100592rs14016510 VPS13A, AGTPBP1, AUH, CAMK4, CDC14B, CDC42SE2, CFC1B, CKS2, CTSL2, DAPK1, FANCC, FBP1, GADD45B, GNAQ, HABP4, HINT1, ISCA1, LOC427470, LOC770548, MIR1456, MIR23B, MIR24-2, MIR27B, MIR7-1, MIR7439, NAA35, NFIL3, NREP, NTRK2, PTCH1, REEP5, RMI1, ROR2, SEMA4D, SLC25A46, SPINZ, STARD4, SYK, TLE4, WDR36, ZCCHC6 2176,02387,719113,769125,790140,660145,617153,135165,390197,067219,311277,332291,087297,203299,152304,979320,390332,352332,687362,742402,941423,299493,436631,537647,587Gga_rs15179992GGaluGA181809Gga_rs15179999Gga_rs10732124Gga_rs15180005Gga_rs15180007GGaluGA181823Gga_rs16176404Gga_rs15180023Gga_rs15180012Gga_rs15180032Gga_rs15180041Gga_rs16176409Gga_rs16176412GGaluGA181852Gga_rs16176425GGaluGA181865GGaluGA181868GGaluGA181877Gga_rs14281175Gga_rs13602346Gga_rs14281291Gga_rs16176824GGaluGA182048rs15179992rs312621287rs15179999rs10732124rs15180005rs15180007rs315641745rs16176404rs15180023rs15180012rs15180032rs15180041rs16176409rs16176412rs314825899rs16176425rs314965954rs313888034rs316891294rs14281175rs13602346rs14281291rs16176824rs312963281 PADI3, PADI1, PADI2, SDHB, MRPS16, PARK7, UTS2, PER3, VAMP3, PHF13, ZBTB48, ICMT, RPL22 Sub-networks 2, 3, 4, 5, 8 and 11 each had several SNPs in the same LD block on one chromosome, which interacted with a single SNP on another chromosome. [score:1]
The color of the edge indicates the type of epistatic effect (AA = red; AD = purple; DA = blue; DD = green) Table 3 The SNPs on GGAZ interacted with the SNPs on GGA21, and the Refgenes in the two important regions Chr Position Locus RS# Refgenes Z37,246,32137,440,77037,562,58238,066,34638,424,44838,545,04438,795,33939,120,19839,189,94639,223,66839,256,77039,415,37840,393,05840,411,58540,514,08541,304,56145,300,03045,695,92746,745,968Gga_rs14765324Gga_rs16768474Gga_rs14765605Gga_rs16768723Gga_rs14766107GGaluGA351567Gga_rs16047676Gga_rs16781643Gga_rs14745723Gga_rs16131986Gga_rs14787078Gga_rs16781713Gga_rs14787751Gga_rs16782083Gga_rs16754179Gga_rs16132921Gga_rs14015526GGaluGA352176Gga_rs14016510rs14765324rs16768474rs14765605rs16768723rs14766107rs317567123rs16047676rs16781643rs14745723rs16131986rs14787078rs16781713rs14787751rs16782083rs16754179rs16132921rs14015526rs316100592rs14016510 VPS13A, AGTPBP1, AUH, CAMK4, CDC14B, CDC42SE2, CFC1B, CKS2, CTSL2, DAPK1, FANCC, FBP1, GADD45B, GNAQ, HABP4, HINT1, ISCA1, LOC427470, LOC770548, MIR1456, MIR23B, MIR24-2, MIR27B, MIR7-1, MIR7439, NAA35, NFIL3, NREP, NTRK2, PTCH1, REEP5, RMI1, ROR2, SEMA4D, SLC25A46, SPINZ, STARD4, SYK, TLE4, WDR36, ZCCHC6 2176,02387,719113,769125,790140,660145,617153,135165,390197,067219,311277,332291,087297,203299,152304,979320,390332,352332,687362,742402,941423,299493,436631,537647,587Gga_rs15179992GGaluGA181809Gga_rs15179999Gga_rs10732124Gga_rs15180005Gga_rs15180007GGaluGA181823Gga_rs16176404Gga_rs15180023Gga_rs15180012Gga_rs15180032Gga_rs15180041Gga_rs16176409Gga_rs16176412GGaluGA181852Gga_rs16176425GGaluGA181865GGaluGA181868GGaluGA181877Gga_rs14281175Gga_rs13602346Gga_rs14281291Gga_rs16176824GGaluGA182048rs15179992rs312621287rs15179999rs10732124rs15180005rs15180007rs315641745rs16176404rs15180023rs15180012rs15180032rs15180041rs16176409rs16176412rs314825899rs16176425rs314965954rs313888034rs316891294rs14281175rs13602346rs14281291rs16176824rs312963281 PADI3, PADI1, PADI2, SDHB, MRPS16, PARK7, UTS2, PER3, VAMP3, PHF13, ZBTB48, ICMT, RPL22 Sub-networks 2, 3, 4, 5, 8 and 11 each had several SNPs in the same LD block on one chromosome, which interacted with a single SNP on another chromosome. [score:1]
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