Ask about this productRelated genes to: WDR13 antibody
- Gene:
- WDR13 NIH gene
- Name:
- WD repeat domain 13
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-11
- Date modifiied:
- 2015-08-26
Related products to: WDR13 antibody
Related articles to: WDR13 antibody
- Peanut (Arachis hypogaea) is an economically important legume crop, but a comprehensive understanding of its gene expression dynamics across developmental stages remains limited. To address this gap, we constructed an integrative multi-omics atlas spanning transcriptomic, proteomic, and metabolomic profiles across 22 primary vegetative and reproductive tissues. We identified 53 030 expressed genes at the transcript level, 12 826 with protein evidence, and 2035 metabolites. Among these, 2147 genes encode novel proteins, and 274 produce microproteins. Functional analyses identified WDR13, TANGO, RPP13, DEF3, SLR1-BP, and SLE2 as key genes involved in development and stress responses. Co-expression analysis grouped genes into 24 modules, many of which exhibited tissue-specific expression patterns. Pathway enrichment and correlation network analyses further highlighted the critical roles of the IAA and ARF gene families in hormone signaling and cell growth, particularly in peg development. To facilitate data accessibility and downstream research, we developed PeanutOmics (https://cgm.sjtu.edu.cn/PeanutOmics), a user-friendly web platform that integrates multi-omics datasets with advanced analytical tools. This atlas offers a valuable resource for understanding gene and metabolite regulation in peanut and lays the groundwork for advanced molecular breeding to improve crop productivity. - Source: PubMed
Publication date: 2025/11/22
Xue HongzhangZhao KunkunDong XiaoruiMa QianHu SaSaCao ZenghuiShu YangLi YanzheHuang XiaoxiangZhao KaiQiu DingShao WenguangRen RuiLi ZhongfengGong FangpingMa XingliWei ChaochunYin Dongmei - The fat tail is a phenotype that divides indigenous Iranian sheep genetic resources into two major groups. The objective of the present study is to refine the map location of candidate regions associated with fat deposition, obtained via two separate whole genome scans contrasting thin and fat tail breeds, and to determine the nature of the selection occurring in these regions using a hitchhiking approach. Zel (thin tail) and Lori-Bakhtiari (fat tail) breed samples that had previously been run on the Illumina Ovine 50 k BeadChip, were genotyped with a denser set of SNPs in the three candidate regions using a Sequenom Mass ARRAY platform. Statistical tests were then performed using different and complementary methods based on either site frequency (F and Median homozygosity) or haplotype (iHS and XP-EHH). The results from candidate regions on chromosome 5 and X revealed clear evidence of selection with the derived haplotypes that was consistent with selection to near fixation for the haplotypes affecting fat tail size in the fat tail breed. An analysis of the candidate region on chromosome 7 indicated that selection differentiated the beneficial alleles between breeds and homozygosity has increased in the thin tail breed which also had the ancestral haplotype. These results enabled us to confirm the signature of selection in these regions and refine the critical intervals from 113 kb, 201 kb, and 2831 kb to 28 kb, 142 kb, and 1006 kb on chromosome 5, 7, and X respectively. These regions contain several genes associated with fat metabolism or developmental processes consisting of and (OAR5), and (OAR7), , , , , , , and (OAR X), and each of which could potentially be the actual target of selection. The study of core haplotypes alleles in our regions of interest also supported the hypothesis that the first domesticated sheep were thin tailed, and that fat tail animals were developed later. Overall, our results provide a comprehensive assessment of how and where selection has affected the patterns of variation in candidate regions associated with fat deposition in thin and fat tail sheep breeds. - Source: PubMed
Publication date: 2022/05/31
Moradi Mohammad HosseinNejati-Javaremi ArdeshirMoradi-Shahrbabak MohammadDodds Ken GBrauning RudigerMcEwan John C - Investigating novel genetic variants involved in intellectual disability (ID) development is essential. X-linked intellectual disability (XLID) accounts for over 10% of all cases of ID in males. XLID genes are involved in many cellular pathways and processes. Some of them are not specific to the development and functioning of the neural system. The implementation of exome sequencing simplifies the search for novel variants, especially those less expected. Here, we describe a nonsense variant of the XLID gene, . The mutation c.757C>T (p.Arg253Ter) was uncovered by X-chromosome exome sequencing in males with a familial form of intellectual disability. Quantitative PCR (qPCR) analysis showed that variant c.757C>T caused a significant decrease in expression in the patient's fibroblast. Moreover, it dysregulated other genes linked to intellectual disability, such as , , , and . The obtained results indicate the pathogenic nature of the detected variant and suggest that the gene interacts with other genes essential for the functioning of the nervous system, especially the synaptic plasticity process. - Source: PubMed
Publication date: 2021/11/28
Rzońca-Niewczas SylwiaWierzba JolantaKaczorowska EwaPoryszewska MilenaKosińska JoannaStawiński PiotrPłoski RafałBal Jerzy - WDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Lepr mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13 mice using hepatotoxin CCl. In the present study we report slower hepatic regeneration in Wdr13 mice as compared to their wild type littermates after CCl administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13 mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl- administered Wdr13 mice, causing de novo lipogenesis. The slower hepatic regeneration observed in CCl administered Wdr13 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway. - Source: PubMed
Publication date: 2020/11/13
Mishra Arun PrakashSiva Archana BGurunathan ChandrashekaranKomala YLakshmi B Jyothi - Endometrial hyperplasia (EH) is a condition where uterine endometrial glands show excessive proliferation of epithelial cells that may subsequently progress into endometrial cancer (EC). Modern lifestyle disorders such as obesity, hormonal changes and hyperinsulinemia are known risk factors for EH. A mouse strain that mimics most of these risk factors would be an ideal model to study the stage-wise progression of EH disease and develop suitable treatment strategies. Wdr13, an X-linked gene, is evolutionarily conserved and expressed in several tissues including uteri. In the present study, Wdr13 knockout female mice developed benign proliferative epithelium that progressed into EH at around one year of age accompanied by an increase in body weight and elevated estradiol levels. Molecular characterization studies revealed increase in ERα, PI3K and a decrease in PAX2 and ERβ proteins in Wdr13 mutant mice uteri. Further, a decrease in the mRNA levels of cell cycle inhibitors, namely; p21 and cyclin G2 was seen. Leukocyte infiltration was observed in the uterine tissue of knockout mice at around 12 months of age. These physiological, molecular and pathological patterns were similar to those routinely seen in human EH disease and demonstrated the importance of WDR13 in mice uterine tissue. Thus, the genetic loss of Wdr13 in these mice led to mimicking of the human EH associated metabolic disorders making Wdr13 knockout female mice a potential animal model to study human endometrial hyperplasia. - Source: PubMed
Publication date: 2020/09/03
Singh ShaluPavuluri SivapriyaJyothi Lakshmi BBiswa Bhim BVenkatachalam BharathiTripura ChaturvedulaKumar Satish