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
- The current treatment strategies for myocardial infarction (MI) mainly focus on recanalization of infarct-related arteries to alleviate myocardial damage. In contrast, the role of promoting microangiogenesis has not received sufficient attention. Lysine crotonylation (Kcr), a novel posttranslational protein modification, has an unclear role in revascularization following MI. - Source: PubMed
Publication date: 2026/07/24
Zhang YanweiBai JiayuZhang LijieSun BinWang HaoWang SiyuLiu JieLiu TongLi HaodongZhang YingFan ShashaGong ManyuZhang YongZhang Ying - - Source: PubMed
Publication date: 2026/08/04
Murthy DivyaAttri Kuldeep SShukla Surendra KThakur RaviChaika Nina VHe ChunboWang DezhenJha KanupriyaDasgupta AneeshaKing Ryan JMulder Scott ESouchek JoshuaGebregiworgis TeklabRai VikantPatel RohitHu TuoRana SandeepKollala Sai SundeepPacheco CamilaGrandgenett Paul MYu FangKumar VikasLazenby Audrey JBlack Adrian RUlahannan SusannaJain AjayEdil Barish HKlinkebiel David LPowers RobertNatarajan AmarnathHollingsworth Michael AMehla KamiyaLy QuanChaudhary SarikaHwang Rosa FWellen Kathryn ESingh Pankaj K - Acetate is the metabolic precursor of acetyl-coenzyme A (CoA), fuelling histone acetylation. - Source: PubMed
Publication date: 2026/07/31
Chen Jie-YingJi Yu-ChenWu Chen-HuiChen Jun-GuangZeng Hui-XianXie ChenFang Jian-HongZhuang Shi-Mei - Acyl-CoA synthetase short chain family member 2 (ACSS2) catalyzes the conversion of acetate to acetyl-CoA. Here we show that expression is markedly elevated in all stages of human colorectal cancer (CRC), and silencing or genetic ablation leads to a marked reduction in CRC tumor load in allograft and xenograft models and CRC models induced by epithelial deletion or azoxymethane/dextran sodium sulfate treatment. Tumors with ACSS2 depletion exhibit robust DNA damage, excessive apoptosis, and increased recruitment of macrophages and CD8 T cells to the tumor microenvironment. Treatment with a small-molecule ACSS2 inhibitor markedly suppresses tumor growth in allograft/xenograft and -mutant CRC models. ACSS2 promotes tumor cell growth by blocking DNA damage and apoptosis under nutritional stress. Collectively, these data indicate that the conversion of acetate to acetyl-CoA by ACSS2 is required for CRC progression and ACSS2 is a potential druggable target for CRC management. - Source: PubMed
Publication date: 2026/07/21
Wang LeiDougherty UrszulaHe WenliangGao LuMuefong CalebSarkar RajeshDu JieShergill ArdamanLin HeningBissonnette MarcLi Yan Chun - Acetyl-CoA is a central metabolite that links energy status to transcriptional regulation through protein acetylation, yet its functions in skeletal biology depend strongly on subcellular compartmentalization. Because acetyl-CoA does not freely traverse biological membranes, its mitochondrial, cytosolic, and nuclear pools are maintained through compartment-specific synthesis and exchange routes, including the citrate-SLC25A1-ACLY axis, acetylcarnitine/carnitine cycling, acetate-dependent ACSS2 activity, and local nuclear enzyme activity. This review synthesizes current evidence that three conserved modules, including glycolytic/PDC-driven mitochondrial production, CIC/ACLY-mediated citrate export, and HAT-dependent acetylation, connect carbon flux with skeletal cell fate. However, lineage-specific outcomes are shaped by local acetyl-CoA availability, acetyltransferase context, and the transcription-factor landscape, including RUNX2 (osteogenesis), SOX9 (chondrogenesis) and NFATc1 (osteoclastogenesis). Critically, compartmentalized acetyl-CoA dysregulation can contribute to different pathological states: excess acetyl-CoA supply is linked to ACLY/FAO-driven cartilage catabolism and osteoclast resorption, whereas insufficient nucleocytosolic supply is associated with impaired regenerative programs in aged or inflamed bone. This duality argues for context-specific therapeutic strategies that either restrain excess acetyl-CoA flux or restore deficient pools. We propose that the translational bottleneck is not target identification but delivery precision, advocating for localized metabolite supplementation, cell-selective ACLY/FAO inhibitors, and spatial acetylome mapping to deconvolute cell-type-specific fluxes. Moving beyond broad HDAC/HAT modulation toward compartment-resolved strategies will be essential for translating acetyl-CoA biology into effective skeletal therapies. - Source: PubMed
Publication date: 2026/07/17
Yang QianyuShi RunlinZhang ChenyangSun WeiChen Guangjin