Ask about this productRelated genes to: TMEM166 antibody
- Gene:
- EVA1A NIH gene
- Name:
- eva-1 homolog A, regulator of programmed cell death
- Previous symbol:
- TMEM166, FAM176A
- Synonyms:
- FLJ13391
- Chromosome:
- 2p12
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-26
- Date modifiied:
- 2016-02-15
Related products to: TMEM166 antibody
Related articles to: TMEM166 antibody
- Renal fibrosis is a common pathological hallmark of chronic kidney disease (CKD), and ultimately leads to end-stage renal disease. ER-stress and TGF-β signaling pathway activation play critical roles in renal fibrosis, but the precise mechanisms underlying the intricate interplay between ER-stress and TGF-β signaling pathway remain ambiguous. Our previous study has demonstrated that EVA1A responds to ER-stress to regulate hematopoietic stem cell regeneration; However, the function of EVA1A in renal fibrosis remains unexplored. - Source: PubMed
Publication date: 2026/01/25
Gao QiongdanWang ZhenkunFu YutingLin ShuyiLiu HaipingZhou YuanyuanWei YifeiJu ZhenyuZhou LiliLiu Bo - To investigate the role of transmembrane protein EVA1A in liver lipid metabolism and development of non-alcoholic fatty liver disease (NAFLD). - Source: PubMed
Xu JiayiYang DiZang KailaiChu MengenZhao QingyaoLi QingLu SenChen XiuliLi Ning - Hepatic lipid dysregulation drives metabolic dysfunction-associated steatotic liver disease (MASLD); nonetheless, the precise regulatory mechanisms remain incompletely elucidated. In this study, we examine the function of EVA1A, a known hepatocellular carcinoma tumor suppressor, in hepatic lipid metabolism. Hepatic EVA1A was markedly down-regulated in individuals diagnosed with MASLD, as well as in mice subjected to a high-fat diet. Hepatocyte-specific knockout of in mice resulted in significant hepatic steatosis, accompanied by disrupted fatty acid metabolism, marked by increased fatty acid uptake and compromised β-oxidation, while hepatic Eva1a overexpression reversed these metabolic changes and largely alleviated fatty liver in ob/ob mice. Mechanistically, EVA1A deficiency activates mTORC1 (mechanistic target of rapamycin complex 1)-PPARγ2 (peroxisome proliferator-activated receptor γ2) signaling to up-regulate CD36 transcription. Concurrently, it transcriptionally represses the S-depalmitoylase APT1 while enhancing palmitoyl acyltransferases ZDHHC4/5, boosting CD36 palmitoylation. This dual action promotes CD36 plasma membrane localization for fatty acid uptake, reducing its mitochondrial distribution and impairing β-oxidation. Collectively, these results establish EVA1A as an essential regulator of hepatic lipid homeostasis, coordinating fatty acid uptake and β-oxidation by modulating CD36 expression and palmitoylation. Therefore, targeting the EVA1A-CD36 axis represents a promising therapeutic strategy for MASLD. - Source: PubMed
Publication date: 2025/11/25
Yang DiLi LianhuiZang KailaiMa WanyongYang YulingSun YaniZhang BingqiangGong ZunshuangYu MingkangDu QiyuanLiu XiaokunWang ZheXu QiyueLi Ning - - Source: PubMed
Publication date: 2025/10/11
Zhu ChenglinZhang QiFan HaoGuo BohongWang Honggang - Guangxi indigenous chickens represent valuable genetic resources characterized by diverse phenotypic features, disease resistance, and superior meat quality, making them ideal breeding materials for modern breeding systems. Elucidating the genetic basis underlying these traits in Guangxi indigenous chickens is crucial for further advancements in breeding programs. In the current study, using whole-genome sequencing, we performed comprehensive genomic analyses to characterize the genetic diversity, population structure, demographic history and selection signatures for seven Guangxi indigenous chicken breeds and two commercial breeds. The results of genetic diversity indices and effective population size demonstrated Guangxi indigenous chicken breeds maintain significantly higher genetic diversity and have undergone less intensive artificial selection than commercial breeds. Population genetic analyses revealed obvious geographic stratification, dividing Guangxi chicken breeds into southern and northern clusters. Southern populations showed closer genetic affinity to red junglefowl (Gallus gallus spadiceus) than northern populations, suggesting differential selection patterns. Genome-wide selection scans identified strong signals between southern and northern populations, uncovering genes associated with pigmentation (BCO2, SOX10, GRM5, MC1R, MITF, EDN3), body size (IGF1, POU1F1, CDH12) and egg production (AKT3, WDR25). Additionally, comparative genomic analysis with commercial breeds identified divergent selection at loci governing genes related to growth, reproduction, disease resistance and environmental adaptability, such as IGF1, LRP1B, GLI3, CDH7, KIF18A, ROBO2, EVA1A, IKZF1, GRID2, and EPHA7. These selection patterns likely reflect the unique genomic features of Guangxi indigenous chickens, shaped by ecological adaptations, traditional husbandry practices, and consumer preferences. Our findings offer new perspectives on the genetic architecture of Guangxi indigenous chickens, facilitating their conservation and utilization in modern breeding programs. - Source: PubMed
Publication date: 2025/09/11
Yang ZhuliangXu WenwenLiu YongcuiSun TiantianXiao CongZou LeqinZeng LinghuDeng JixianYang Xiurong