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
- Sepsis-induced myocardial injury (SIMI) is a severe complication of sepsis with limited mechanism-based therapies. We investigated whether Relaxin-3 attenuates SIMI and modulates macrophage inflammatory responses. - Source: PubMed
Publication date: 2026/05/05
Yang YuxinLiu XiaoqiXue JiaxinYun ChengchengDou YingWang JingzhiZhang Xiaohui - Osteoporosis (OP) is a systemic metabolic bone disorder. The excessive activation of osteoclasts (OCs) leads to a decrease in bone mass and damage to the bone microstructure, which plays a crucial role in OP. β-Hydroxybutyrate (BHB), the main component of ketone bodies, not only serves as an ancillary fuel substituting for glucose but also induces anti-oxidative, anti-inflammatory, and cardioprotective features via binding to several target proteins, including histone β-hydroxybutyrylation (Kbhb). Recent research has found that BHB has a positive therapeutic effect on OP, but the underlying molecular mechanism remains unclear. In this study, we established osteoporosis (OP) animal models induced by estrogen deficiency and type 2 diabetes using ovariectomized (OVX) and db/db mice, respectively, and administered BHB to OP mice via free drinking in vivo. Our results indicated that BHB increased bone mineral density (BMD), improved bone microstructure, and inhibited the OC formation. Additionally, BHB upregulated the levels of PanKbhb, H3K9bhb, and H3K27bhb modifications in the bone tissue of OP mice. In vitro, we found that BHB or β-hydroxybutyryl-CoA (BHB-CoA) could inhibit RANKL-induced OC differentiation and bone resorption, and upregulate histone Kbhb levels in a concentration-dependent manner. Furthermore, the effects of BHB or BHB-CoA-induced histone Kbhb were reversed by inhibiting the activity of Acyl-CoA synthetase short-chain family member 2 (ACSS2) or histone acyltransferase P300. In summary, our data reveal that BHB may alleviate bone loss caused by estrogen deficiency and type 2 diabetes through ACSS2/P300-induced histone Kbhb. - Source: PubMed
Publication date: 2026/04/30
He YanqiuMou ChenglongTang MinLuo LiZhou TingtingCheng XiLi DongzeLuo ChangfangGuo ManHu JinboLi QifuWan QinDeng LiyunLi YueZhang HaiqiangNi QiongyuXu YongGao ChenlinHuang Wei - Cardiovascular diseases increase with aging and are closely linked to metabolic dysfunction and kidney disease through the cardiovascular-kidney-metabolic axis, but the underlying molecular mechanisms remain unclear. Accumulating evidence suggests that vascular endothelial cells (ECs) are particularly vulnerable to aging stressors, such as DNA damage. We investigated whether EC DNA damage drives cardiovascular-kidney-metabolic dysfunction. - Source: PubMed
Publication date: 2026/04/30
Ito WataruNakamichi RanHishikawa AkihitoYoshimoto NorifumiNishimura Erina SugitaHama Eriko YoshidaMaruki TomomiIwabuchi SeieiYoshida RyutoToda MasataroKosugi ShotaroYamaguchi ShintaroKanda TakeshiHashiguchi AkinoriItoh HiroshiHayashi Kaori - Cognitive function impairment following sleep deprivation (SD) can induce significant aftereffects. Elevated calmodulin (CaM) expression following stroke causes calcium overload-a key contributor to cognitive function impairment. Trifluoperazine (TFP), a CaM inhibitor, reduces CaM overexpression following ischemic stroke. However, it remains unclear whether TFP has influences on cognitive function impairment following SD. We administered TFP to rats subjected to SD. TFP treatment in SD rats reduced cerebral CaM expression and alleviated cognitive function impairment. Improved cognitive function was coincident with increased CaM protein levels and reduced acetyl-CoA synthetase 2 (ACSS2) protein levels after SD. TFP treatment reversed these changes. Our results showed that TFP administration in rats inhibited CaM protein following SD by upregulating ACSS2 protein expression, thereby improving ACSS2-related autophagy and alleviating cognitive function impairment. Consequently, this treatment may promote cerebral cognitive function recovery after SD. - Source: PubMed
Publication date: 2026/03/30
He CaijunWang BiaoChen XuanyuXu JiachengYang YaxinYuan Mei - Exposure to coke oven emissions (COEs) is an important environmental factor in lung cancer. A previous study revealed that 20 μg/mL COE exposure for 120 days could induce malignant transformation of lung epithelial cells. However, the underlying mechanism remains unclear. The epigenetic regulation of long noncoding RNAs (lncRNAs) plays an important role in carcinogenesis. Changes in lncRNA expression during COE-induced malignant transformation were detected, highlighting the importance of gene-environment interactions in cancer. Here, we identified that was downregulated in COE-induced malignant transformation of lung epithelial cells. Interestingly, this reduction was found to have a gradient effect on different stages of cells of COE exposure. Moreover, we found that downregulation of expression in lung cancer was related to patients' poor prognosis. Phenotypic studies have demonstrated that suppressed lung cancer cell proliferation in vitro and in vivo. Further mechanistic studies revealed that directly interacts with ACSS2, an important enzyme responsible for synthesizing acetyl-CoA, leading to abnormal acetyl-CoA metabolism and affecting COE-induced lung carcinogenesis. COE-induced malignant transformed cells or cells with the knockdown of showed significantly increased fatty acid and cholesterol levels, while normal lung epithelial cells or cells with overexpression of showed substantially decreased fatty acid and cholesterol levels. Moreover, transfection of ACSS2 into cells with overexpressing could rescue the induced cell phenotype. Our findings link regulated acetyl-CoA metabolism with COE-induced malignant transformation and imply that could be an important biomarker for early intervention and diagnosis of lung cancer. - Source: PubMed
Publication date: 2025/12/21
Ju QiangLi XinmeiWu ZhaoxuZhang PimeiChen HongguangJi JingGao WeiZheng YuxinYu DiankeZhao Yanjie