ACSF2
- Known as:
- ACSF2
- Catalog number:
- 001043A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACSF2
Related genes to: ACSF2
- Gene:
- ACSF2 NIH gene
- Name:
- acyl-CoA synthetase family member 2
- Previous symbol:
- -
- Synonyms:
- FLJ20920, ACSMW
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2015-08-26
Related products to: ACSF2
Related articles to: ACSF2
- Ruminant epithelia preferentially catabolize butyrate to fuel metabolism, yet the mechanism by which the rumen epithelium establishes this preference remains unclear. Here, we identify ACSF2 as a mitochondrial acyl‑CoA synthetase (ACS) that catalyzes the activation of butyrate to butyryl‑CoA, thereby enabling rumen butyrate preference. We found that ACSF2 is markedly enriched in the forestomachs across ovine organs, with expression far exceeding other ACSs in the rumen epithelium, and it is rising during postnatal establishment of fermentative function. Single‑cell transcriptomics and immunostaining localize ACSF2 to the mitochondria‑rich layers, where it is co‑expressed in mitochondria with ketogenesis genes, notably the rate‑limiting enzyme HMGCS2. Further gain‑ and loss‑of‑function experiments show that ACSF2 activates butyrate to butyryl‑CoA, enhances butyrate‑supported growth, and is required for efficient butyrate consumption, cell fitness, and ketogenesis under butyrate‑dependent conditions. These findings define ACSF2 as a key mitochondrial gatekeeper for butyrate utilization in the rumen epithelium, providing a molecular mechanism for butyrate‑biased energy metabolism during rumen maturation. - Source: PubMed
Publication date: 2026/08/02
Song MingmeiQin JingTian JunruZhang KaiZhang YaliXiang Xiao'eZhu WeiyunMao ShengyongLiu JunhuaHuang Zan - Therapeutic resistance to cytarabine (Ara-C), a cornerstone of acute myeloid leukemia (AML) therapy, remains an unmet clinical need. Here, we identify ACSF2 as a key metabolic determinant of Ara-C resistance. ACSF2 inhibition suppresses Ara-C-resistant AML cell proliferation, restores Ara-C sensitivity in vitro and in vivo. Mechanistically, ACSF2 inhibition impairs cholesterol esterification. Therefore, the increased cholesterol accumulation on mitochondrial membranes results in mitochondrial dysfunction, elevated mitochondrial reactive oxygen species (ROS), and suppression of pro-survival ERK signaling. Furthermore, we first established SREBF1 as a direct transcriptional activator of ACSF2 in this context. Notably, the SREBF1 inhibitor fatostatin synergizes with Ara-C against resistant AML with downregulation of ACSF2. These findings define a crucial role of ACSF2 in Ara-C resistance and highlight the SREBF1-ACSF2 axis as a promising therapeutic target for relapsed/refractory AML. - Source: PubMed
Publication date: 2026/07/31
Liao ChenxiWen JinMa XiaoWang NanChen YingLi LeiLiu LingboPeng Danyue - Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising therapeutic strategy for cervical cancer. However, the mitochondrial factors governing ferroptosis sensitivity in this malignancy remain incompletely understood. PET117, a conserved mitochondrial protein, has been implicated in mitochondrial homeostasis, yet its role in ferroptosis regulation and cervical cancer pathophysiology is unknown. Here, we report a novel role of PET117 in regulating ferroptosis. PET117 expression was significantly elevated in cervical cancer tissues and loss of in HeLa cells markedly suppressed erastin- and RSL3-induced ferroptosis. Mechanistically, deficiency attenuated intracellular reactive oxygen species (ROS) accumulation, lipid peroxidation, and iron overload. Mitochondrial proteomics and RNA-seq revealed extensive remodeling of the mitochondrial proteome and ferroptosis-related transcriptional networks upon PET117 depletion. Notably, integrative analysis of mitochondrial and nascent proteomes identified acyl-CoA synthetase family member 2 (ACSF2) as a downstream target of PET117. These findings establish PET117 as a novel regulator of ferroptosis in cervical cancer, thereby linking mitochondrial function to ferroptosis regulation. - Source: PubMed
Publication date: 2026/07/14
Sun QiongWang DandanZhao QingCui YuZhang YiruPi YaoluLiu HuadongWang Zhen - RNA-binding motif 47 (RBM47), a hub gene in atherosclerosis, induced oxidative stress in macrophages in atherosclerosis progression by enhancing ENC1 stability via binding to the AU-rich elements (AREs). However, RBM47 promoted C-to-U editing of multiple genes, such as acyl-CoA synthetase family member 2 (ACSF2), apoB, CD36, CD170, IL-10, oxysterol binding protein like 9, and transmembrane protein 30a (TMEM30A). These genes play important roles in atherosclerosis. Thus, the role of RBM47 in atherosclerosis may be complex. Notably, ACSF2 and HECT and RLD domain containing E3 ubiquitin protein ligase 2 promoted ferroptosis. TMEM30A exhibited a "don't eat me" signal. CD170 decreased ADAMTS13 activity. Recombinant ADAMTS-13 was undergoing phase 3 clinical trials. However, the biological significance of these genes after RNA editing, except for apoB and tight junction protein 1, is unclear. RBM47 also stabilized Axin1, Cullin 3, IL-8, Dickkopf WNT signaling pathway inhibitor 1, Kelch-like ECH-associated protein 1, and IL-10 expression by recognizing the GAUSAW (S = G/C, W = A/U) motif and AREs/GU-rich elements (GREs). However, the role of RBM47 in other genes that contain AREs and GREs, such as apoA-II, ABCA1, HMGCR, IFN-γ, IL-15, low-density lipoprotein receptor, oxidized low-density lipoprotein receptor 1, and programmed cell death 1 ligand 1, is unclear. This review focuses on the role and mechanism of RBM47-mediated genes in atherosclerosis to provide knowledge for new targets. - Source: PubMed
Publication date: 2026/07/23
Hu JingRen ChunlingChen WujunZhong YingjieXu Mantao - Acute myeloid leukemia (AML) is a hematologic malignancy characterized by heterogeneity, poor prognosis, and limited biomarkers for risk prediction. Mitochondria pathway related genes (MPRGs), as central regulators of cellular metabolism and immune microenvironment dynamics, may provide useful information for prognostic assessment and biological characterization in AML. - Source: PubMed
Publication date: 2026/05/19
Dou RuiLi WeiZhang LeiLi DanCheng WeiZhu Zunmin