Ask about this productRelated genes to: ACSS2 antibody
- Gene:
- ACSS2 NIH gene
- Name:
- acyl-CoA synthetase short chain family member 2
- Previous symbol:
- ACAS2
- Synonyms:
- ACS, ACSA, AceCS, dJ1161H23.1
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-17
- Date modifiied:
- 2017-06-13
Related products to: ACSS2 antibody
Related articles to: ACSS2 antibody
- In pigs, ZGA occurs around the 4-cell stage, when embryos move from the oviduct to the uterus. This overlap suggests that embryonic transcription begins as the embryo enters a new local environment. Despite this transition, many porcine in vitro production (IVP) systems provide metabolic supplements from the beginning of culture without considering the post-ZGA period separately. Acetate is a short-chain fatty acid found in the reproductive tract and can be converted into acetyl-CoA, thereby linking metabolism with epigenetic regulation. We therefore examined whether acetate supplementation after the presumed major ZGA period could improve porcine embryo development. Embryos were cultured with acetate after ZGA and assessed for blastocyst development, mitochondrial membrane potential, reactive oxygen species, glutathione, histone acetylation, and expression of survival- and adhesion-related genes. Acetate increased blastocyst formation and was accompanied by higher mitochondrial membrane potential, lower ROS-associated fluorescence, and increased glutathione levels. The treated embryos also showed stronger H3K9ac and H3K27ac signals and increased ACSS2 mRNA expression, together with changes in genes related to chromatin regulation, cell survival, and blastocyst integrity. These results show that acetate supplementation during the post-ZGA period improves porcine embryo development under the present IVP conditions and supports its use as a potential metabolic modulator during this developmental window. - Source: PubMed
Publication date: 2026/06/15
Ha YunjuLee SeungjunKim SeeunKim Min JungCho Jongki - Organelles have been reported to be closely associated with tumor development and progression, but their role in osteosarcoma (OS) remains largely unexplored. Organelle related genes (ORGs) associated with OS prognosis were identified using Cox regression analysis. A prognostic model was subsequently constructed through multivariate Cox regression analysis and validated using an independent dataset. Patients were stratified into high-risk and low-risk groups based on the median risk score. In addition, immune infiltration analysis, enrichment analysis and drug sensitivity evaluation were performed. Finally, in vitro experiments were conducted to validate the potential roles of ORGs in OS. We identified 3 ORGs (ACSS2, CLTCL1, and PLD3) that were significantly associated with OS prognosis. A novel 3 ORG signature was established, which effectively stratified patients into high-risk and low-risk groups with distinct survival outcomes. This signature served as an independent prognostic factor. The areas under the receiver operating characteristic (ROC) curve for the 1-, 4-, and 7-year survival rates were 0.66, 0.74, and 0.83, respectively. These findings were further validated using the independent GSE21257 dataset, where the corresponding ROC curve values for the 1-, 4-, and 7-year survival rates were 0.71, 0.80, and 0.68, respectively. Drug sensitivity analysis revealed differential responses to 4 drugs between the risk groups, with the 3 ORGs (ACSS2, CLTCL1 and PLD3) showing positive correlations with 2 drugs (BI_2536, Dactinomycin). Additionally, functional experiments confirmed the role of ACSS2 in OS cell behavior. This novel ORG signature not only provides a valuable tool for patient stratification but also offers insights into the biological processes driving OS progression and potential therapeutic targets. - Source: PubMed
Publication date: 2026/06/17
Sun BingZhu JieyangJiang YiChen SihuiZhang Tao - Diabetic foot ulcers (DFU) is a serious complication of diabetes, and keratinocyte ferroptosis has been shown to accelerate its pathological progression. Chuanglin Ye (CLY), widely used in clinical practice for the treatment of DFU, has been reported to exert anti-inflammation effects and promote skin regeneration. However, its pharmacological mechanisms on DFU remain unclear. - Source: PubMed
Publication date: 2026/06/08
Feng XiaoYi NanZhang CunyuTang LiangYin XindongZhao YaZhu TaiyangZhu JianhuaFeng QianChen WeiweiXia YawenMa Chaoqun - Aging is a major driver of tissue senescence, but little is known about the development of age-unrelated tissue senescence. Here we show that nucleocytosolic acetyl-CoA deficiency in colon epithelial cells, caused by ablation and bacterial depletion, triggers age-independent, p53-dependent colonic senescence leading to severe systemic inflammation. Acetate supplementation, acetate-producing bacterial transplantation, targeted depletion of senescent cells or treatment with lysine deacetylase inhibitors blocks colonic senescence and inflammatory injury. Spontaneous colonic senescence develops following simultaneous deletion of epithelial and , confirming that microbe-derived acetate maintains the epithelial acetyl-CoA pool via ACSS2 to avert colonic senescence. Mechanistically, acetyl-CoA deficiency deprives a cohort of mitochondrial and nuclear proteins of acetylation, leading to increased oxidative stress and DNA repair stress that trigger cellular senescence. Among these proteins, ATP5F1A-K161 acetylation and H4-K5/8 acetylation are required to protect colonic epithelial cells from developing senescence. These observations unveil a previously unknown mechanism that governs colonic senescence. - Source: PubMed
Publication date: 2026/05/19
Du JieSarkar RajeshWang LeiTabrizi Roya AminiGao LuLi YanSidebottom AshleyShah HardikChen MengjieOdenwald MatthewLi Yan Chun - The loss of smooth muscle cell (SMC) contractile phenotype contributes to various diseases including atherosclerosis. However, its metabolic basis is not entirely elucidated. Since the transforming growth factor beta (TGFβ) signaling is among principal regulators of SMC contractility, we studied metabolic regulation of TGFβ signaling in SMCs in vitro and atherosclerotic mouse models and human lesions. We found that TGFβ induced Ac-CoA synthetase 2 (ACSS2)-dependent Ac-CoA production, by suppressing pyruvate dehydrogenase kinase 4 (PDK4). This stabilized R-SMADs and TGFβ receptor 1, preserving SMC contractile phenotype. SMC-specific PDK4 knockout mimicked the effect of TGFβ signaling both metabolically and phenotypically, increasing glucose-derived synthesis of Ac-CoA and SMC contractile phenotype. SMC-specific knockout in knockout mice reduced atherosclerosis. Furthermore, human specimens demonstrated a strong correlation between PDK4 level and atherosclerosis severity. These findings indicate that continuous TGFβ signaling, critical to the maintenance of the normal SMC contractile state and is regulated by PDK4 and carbohydrate metabolism. - Source: PubMed
Publication date: 2026/05/21
Zhang Rong-MoZhu XiaolongBae HosungZhang JiashengLi YanmingChen Pei-YuShen Ying HTellides GeorgeSnyder NathanielJang CholsoonSchwartz Martin AArany ZoltanSimons Michael