Ask about this productRelated genes to: ACSBG1 antibody
- Gene:
- ACSBG1 NIH gene
- Name:
- acyl-CoA synthetase bubblegum family member 1
- Previous symbol:
- -
- Synonyms:
- BGM, FLJ30320, MGC14352, BG1, KIAA0631, hBG1, hsBG
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-08
- Date modifiied:
- 2018-05-03
Related products to: ACSBG1 antibody
Related articles to: ACSBG1 antibody
- Astrocytes are key regulators of lipid metabolism, and dysregulated astrocytic lipid processing is implicated in Parkinson's disease (PD) pathogenesis. Our prior genome-wide screens identified ACSBG1, an astrocyte-enriched acyl-CoA synthetase, as a candidate regulator of α-synuclein (α-Syn) levels. However, how ACSBG1 links lipid reprogramming to inflammatory astrocyte activation and α-Syn pathology remains unknown. We compared the transcriptomic, cytokine, and lipid secretomes of TNF-α and IL-1α stimulated primary astrocytes from wild-type (WT) and knockout (KO) mice. In vivo, we crossed Acsbg1 KO mice with a Thy1-α-Syn PD model to assess behavior, neuroinflammation, synaptic integrity, and α-Syn levels. Following cytokine exposure, KO astrocytes mounted an attenuated inflammatory transcriptional response, secreting significantly fewer inflammatory mediators (e.g., IL-6, RANTES, MIP-3α) and less long-chain Sphingosine 20:1 than WT astrocytes. Importantly, exogenous Sphingosine 20:1 or cytokines from WT reactive astrocytes induced neuronal α-Syn phosphorylation (pS129). deletion in Thy1-α-Syn mice reduced astrogliosis, rescued synaptic and behavioral deficits, and decreased total and pS129-α-Syn. These findings establish ACSBG1 as a key regulator of inflammatory astrocyte signaling that contributes to α-Syn phosphorylation via specific cytokine and lipid mediators, identifying ACSBG1 as a novel therapeutic target for modulating astrocyte-neuron communication in PD. - Source: PubMed
Publication date: 2026/06/08
Kim YoungDooVaidya BhupeshKim JiyoenBitar SaraShajan Femil JosephVerma Ajay KumarYalamanchili Hari KrishnaSingh ShubhamZoghbi Huda Y - Striae gravidarum (SG) is a common skin condition characterized by disrupted dermal extracellular matrix (ECM) homeostasis. Despite its high prevalence, the underlying cellular and molecular pathogenesis remains poorly understood, particularly regarding fibroblast heterogeneity and metabolic dysregulation. - Source: PubMed
Publication date: 2026/05/16
Cheng YuLiang ChenCai ZixinLi ZhuoyuanSun YiDanFu XiujunLi ShuaijunLiu CaiyueWang Chen - Porcine epidemic diarrhea virus (PEDV) poses a significant threat to the global swine industry; however, the host factors that support its replication remain poorly understood. Our previous study showed that myeloid cell leukemia 1 (MCL1) is a pro-PEDV replication cellular factor through genome-scale CRISPR-Cas9-knockout (KO) screening. Nevertheless, the molecular mechanism whereby MCL1 promotes PEDV replication is unclear. In this study, we first demonstrated that MCL1 promotes PEDV replication through its BCL-2 homology (BH) domain. Deletion of MCL1 prevented arachidonic acid (AA) from undergoing β-oxidation which led to the increase of free AA and activation of its secondary metabolic pathways resulting in significant inhibition of PEDV replication. Complementation of MCL1-KO cells with a BH domain fragment of MCL1 restored β-oxidation capacity and rescued PEDV replication. In addition, we identified acyl-CoA synthetase bubblegum family member 1 (ACSBG1) as a novel metabolic regulator that binds to the N-terminus of MCL1, rather than its BH domain, and cooperates with MCL1 to facilitate AA β-oxidation. We further demonstrated that ACSBG1 and MCL1 act together as proviral factors specifically during the replication stage of PEDV infection. In summary, this work reveals a unique and concerted interaction between MCL1 and ACSBG1 that function together to promote PEDV replication by regulating the AA metabolic pathway. - Source: PubMed
Publication date: 2026/04/24
Shang HongqiYang ShanshanSun MinZhao YongxiangGuo RongliWang WeiQian BingxuLi YunchuanHu MiBian XianyuCao QiuxiaLi ChengchengFan BaochaoLi Bin - Lung adenocarcinoma (LUAD) remains a leading cause of cancer‑associated mortality with limited prognostic biomarkers. Fatty acid metabolism (FAM) reprogramming serves a pivotal role in tumor progression; however, the functional importance of specific FAM genes, such as ACSBG1, in LUAD remains elusive. In the present study, transcriptomics data from The Cancer Genome Atlas (n=517) and Gene Expression Omnibus‑GSE13213 (n=117) were analyzed to identify FAM‑related differentially expressed genes (DEGs). Least Absolute Shrinkage and Selection Operator regression and Shapley Additive Explanations (SHAP) interpretable analyses established a prognostic model, and experiments using A549 and H1299 cell lines with ACSBG1 overexpression (OE) and knockdown. Functional assays included Cell Counting Kit‑8, EdU, Transwell and apoptosis analyses. A total of 35 FAM‑related DEGs were identified, which were enriched in PPAR signaling and fatty acid degradation pathways (false discovery rate <0.05). Subsequently, a seven‑gene prognostic model was established, and demonstrated strong predictive power for 1‑, 3‑ and 5‑year survival (area under the curve values: 0.767, 0.769 and 0.700, respectively). SHAP analysis prioritized ACSBG1 as the dominant protective factor, and its low expression was associated with advanced Tumor‑Node‑Metastasis stages and poor survival. Mechanistically, ACSBG1 OE suppressed proliferation, migration and invasion, and promoted apoptosis. Immune profiling revealed ACSBG1 expression was positively correlated with the infiltration of CD4 T cells, CD8 T cells and B cells, suggesting its immunomodulatory potential. In conclusion, to the best of our knowledge, the present study established the first FAM‑based prognostic model for LUAD, and identified ACSBG1 as a novel tumor suppressor through dual mechanisms of metabolic regulation and immune microenvironment modulation. The risk score system established in the current study provides a clinically actionable tool for precision oncology, and ACSBG1‑targeted therapy represents a promising strategy against LUAD progression. - Source: PubMed
Publication date: 2026/03/06
Hu PanxinLi Anan - This study characterized phenotypic distinctions between high- and low-motility sperm from 40-week-old Yufen1 roosters and the alteration in epididymal transcriptional networks underlighting sperm motility. Temperature challenge tests (4 °C and 37 °C) revealed that high-viability sperm maintained significantly better survival rates at both temperatures compared to low-viability samples, and high-motility sperm consistently exhibited lower morphological abnormality rates across temperature conditions (P < 0.05), which was further confirmed by extended fertilization windows (P < 0.05) and produced more fertilized eggs (P < 0.05) compared to the low-motility group. Transcriptomic analysis of the epididymis showed 723 differentially expressed genes between the low- and high- motility groups, with functional enrichment indicating significant alterations in lipid metabolism pathways and ATP synthesis-related processes. Accordingly, genes related to fat deposition such as acyl-CoA synthetase bubblegum family member 1 (ACSBG1), glycerate kinase (GLYCTK), and CDP-diacylglycerol synthase 1 (CDS1) were downregulated (all P < 0.05), whereas the mRNA level of β-oxidation gene acyl-coenzyme A thioesterase 6 (ACOT6) was increased (P < 0.05) in the high motility group as compared to the low motility group. In addition, when compared to the low motility group, the high motility semen exhibited decreased levels of both reactive oxygen species (ROS) and malondialdehyde in seminal plasma (both P < 0.05). In conclusion, the maintenance of sperm motility is associated with lipid metabolism remodeling, where these metabolic adaptations enhance ATP production while simultaneously reducing ROS generation in Yufen1 roosters. - Source: PubMed
Publication date: 2026/01/08
Li JiweiLiu PingquanZhang JuanTian YadongSun GuirongKang XiangtaoGu YalingLi Donghua