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
- 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 - Brain metastasis in breast cancer patients represents a terminal disease stage, with median survival typically measured in months. Tumors that colonize the brain must adapt to its unique microenvironment, such as high acetate levels. Primary brain tumor cells enhance acetate conversion to acetyl-CoA through phosphorylation of acetyl-CoA synthetase 2 (ACSS2) by cyclin-dependent kinase 5 (CDK5), a process regulated by the nutrient sensor O-GlcNAc transferase (OGT). In this study, we showed that brain-metastatic breast cancer cells exhibited elevated O-GlcNAc, OGT, and phosphorylated ACSS2 (Ser267) compared to their parental counterparts. Both OGT and CDK5 were essential for in vivo tumor growth in the brain, and ACSS2 and a phospho-mimetic S267D mutant drove progression of brain metastatic breast cancer. Mechanistically, ACSS2 supported tumor cell survival by suppressing ferroptosis through E2F1-dependent transcription of the anti-ferroptotic protein SLC7A11. Treatment with brain-penetrant ACSS2 inhibitor AD-5584 induced ferroptosis and significantly suppressed breast cancer brain metastatic growth ex vivo and in vivo. Together, these findings identify ACSS2 as a key metabolic regulator of brain-metastatic breast cancer survival and a promising target for ferroptosis-inducing therapies. - Source: PubMed
Publication date: 2026/04/22
Young Riley GEsquea Emily MCiraku LorelaMerzy JessicaAhmed Nusaiba NTalarico Alexandra NKaruppiah MangalamMedori Sophia MWarade Rujula PGocal WiktoriaDick AlexejSimone Nicole LReginato Mauricio J - Yak milk is recognized for its superior nutritional quality, yet the biological basis underlying its high milk protein content remains poorly understood, particularly regulatory mechanism of small intestine. This study compared the major nutrients and amino acid composition of raw milk among yaks, cattle-yaks and cows, revealing the characteristics of high protein and rich amino acids in yak milk. We annotated 16 major cell types from a total of 27,026 cells by constructing the first single-cell transcriptome atlas of yak small intestine. Among them, intestinal stem cells and tuft cells exhibited strong proliferation and differentiation potential, contributing to the maintenance of efficient protein absorption. Our multi-strategy GWAS framework by integrating genomics and scRNA-seq data further identified candidate genes associated with milk protein content (SCP2, ETV6, ACSS2, and WWOX), which are mainly involved in amino acid utilization and energy regulation. Notably, WWOX was consistently identified across multiple analyses. It may enhance protein absorption efficiency in the small intestine, thereby providing sufficient substrates for milk protein synthesis and ultimately increasing milk protein content in yaks. In summary, these findings demonstrate that functional specialization of the small intestine contributes to enhanced milk protein content in yaks and highlight the importance of integrating phenotypic, cellular, and genetic data to understand complex traits. This work provides a novel perspective on the regulation of milk protein and offers potential targets for genetic improvement of milk quality in yaks and other ruminants. - Source: PubMed
Publication date: 2026/04/09
Huang ChunYu QinranMa XiaomingChu MinBao PengjiaGuo XianLiang ChunnianYan Ping - Acetate serves as an alternative carbon source in nutrient-limited tumors, yet its role in supporting nucleotide biosynthesis remains poorly understood. Here, we identify the mitochondrial enzyme ACSS1 as a key metabolic driver in mantle cell lymphoma (MCL), diffuse large B-cell lymphoma (DLBCL), and chronic lymphocytic leukemia (CLL). ACSS1 is frequently overexpressed and catalyzes the conversion of acetate to mitochondrial acetyl-CoA, sustaining oxidative metabolism and biosynthesis under nutrient stress. Genetic silencing of ACSS1 impairs mitochondrial respiration and disrupts acetate incorporation into acetyl-CoA, TCA cycle intermediates, glutamate, and aspartate, while markedly reducing C-acetate labeling of dihydroorotate and orotate, intermediates in de novo pyrimidine synthesis. Untargeted metabolomics reveal enrichment of pyrimidine biosynthesis pathways in ACSS1-high cells. Notably, acetate or uridine supplementation rescues the growth of ACSS1-deficient cells, confirming a functional link between acetate metabolism and nucleotide synthesis. Importantly, in vivo studies using two different MCL xenografts demonstrate that ACSS1 knockdown profoundly suppresses tumor growth, indicating that ACSS1 is required not only for metabolic adaptation of lymphoma cells in vitro but also in vivo. Collectively, our results uncover an ACSS1-dependent mitochondrial acetate-pyrimidine axis that sustains lymphoma growth and represents a previously unrecognized therapeutic vulnerability. - Source: PubMed
Publication date: 2026/04/07
Basappa JohnveslyGoldman Aaron RLobello CosimoWang ShengchunRushmore DavidMelnikov OlgaSen Neil VMallikarjuna Vinay SJain PriyankaEdalati MasoudNelson David SCai Kathy QLu PinNejati RezaBorghaei HosseinGupta Pradeep KNath KavindraWellen Kathryn EWasik Mariusz A