ACSL5
- Known as:
- ACSL5
- Catalog number:
- 001048A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACSL5
Related genes to: ACSL5
- Gene:
- ACSL5 NIH gene
- Name:
- acyl-CoA synthetase long chain family member 5
- Previous symbol:
- FACL5
- Synonyms:
- ACS5, ACS2
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-14
- Date modifiied:
- 2017-06-13
Related products to: ACSL5
Related articles to: ACSL5
- Emerging evidence has shown that fatty acid metabolism is closely associated with autoreactive T cells in autoimmunity, but its function in Sjögren's syndrome (SS) is still unclear. Here, we identified acyl-CoA synthetase long-chain family member 5 (ACSL5) as a metabolic checkpoint that drives pathogenic T-cell responses in SS. ACSL5 was upregulated in patients with SS and positively correlated with T-cell infiltration and lipid dysregulation. ACSL5-high T cells presented hyperactive effector activity and a proinflammatory phenotype. Metabolic profiling indicated that ACSL5 increased fatty acid uptake and utilization and promoted fatty acid oxidation (FAO) through peroxisome proliferator-activated receptor alpha (PPARα) in T cells, thereby improving mitochondrial respiratory capacity. Mechanistically, ACSL5 facilitated the nuclear translocation of PPARα and subsequent Mitofusin 2 () transcription, increasing mitochondrial elongation and the formation of mitochondria‒endoplasmic reticulum contacts (MERCs) to influence the FAO and T-cell response. Disruption of the ACSL5/PPARα/MFN2 axis attenuated effector functions and reduced the longevity of pathogenic effector T cells. Pharmacological inhibition of FAO or ACSL5 decreased inflammatory T-cell infiltration and alleviated salivary gland inflammation. Collectively, these findings reveal an ACSL5-centered metabolic program that sustains pathogenic T-cell responses in SS and suggest ACSL5/FAO as a potential therapeutic target. - Source: PubMed
Publication date: 2026/07/13
Ren XinyiYin JunhaoMa XinyiXu JiabaoChen ChangyuHe LeleZhao RuowenXu YuchengPu YipingWang BaoliFu JiayaoZheng Lingyan - Decabromodiphenyl ether (BDE-209) is a widely used flame retardant and persistent environmental contaminant. However, the overlap between predicted BDE-209-related targets and ulcerative colitis (UC)-associated molecular signatures has not been systematically evaluated. - Source: PubMed
Publication date: 2026/07/06
Zhang YueZhang HaiHu DanliZhang HailongWang DaHong ZiyangSu SiChen Ling - Triple-negative breast cancer (TNBC) is highly aggressive and has strong metastatic potential, and effective targeted therapies remain limited. There is growing evidence that the adipocyte microenvironment plays an important role in tumor progression, but its specific mechanism remains to be studied. As a key enzyme for the activation of long-chain fatty acids, the role and regulatory mechanism of ACSL5 in TNBC have not been clarified. - Source: PubMed
Publication date: 2026/07/01
Li YingnanSun XinyiPeng JingMa TengLiu ChanggenWang Haibo - Fat deposition plays an important role in yak metabolism, reproduction, and meat quality, and male yaks are often castrated to facilitate management and improve production performance. The effect of castration on the characteristics of fat deposition in male yaks and the molecular mechanisms of action was explored in this study. The subcutaneous fat thickness in castrated and common male yaks was measured, further the content of fatty acids in yak subcutaneous fat was detected using gas chromatography-mass spectrometer (GC-MS); the transcriptome, metabolome in the yak subcutaneous fat were detected using mRNA-Sequencing, ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS), respectively; the integrative analyses of differentially expressed genes (DEGs), different metabolites (DMs), fatty acids and fat thickness were carried out. The results showed that castration can strengthen the ability of fat deposition and improve the content of fatty acids, especially PUFAs, in male yaks, and both transcriptome and metabolome were significantly different between castrated male yaks and common male yaks. The effect of castration on the male yak fat deposition was closely related to the PPAR signaling pathway, citrate cycle, and insulin resistance. Data suggests that , , , , , , , and may be the crucial control genes for the fat amount in yaks, and that , , and may be the crucial control genes for the polyunsaturated fatty acids (PUFAs) content in yak adipose tissue. Further functional studies will be conducted to determine the specific role of each gene in regulating fat deposition and fatty acid composition in yaks. - Source: PubMed
Publication date: 2026/06/12
Xiong LinPei JieGe QianyunDing ZhiqiangKang YandongChen ChaoWei RuichaoGuo Xian - Colorectal cancer recurrence is largely attributed to dormant tumor cells that evade therapy. The role of organelle metabolism, particularly lipid droplets (LDs) accumulation, in maintaining tumor dormancy remains poorly understood. This study aimed to investigate how LDs contribute to dormancy and to identify key regulatory mechanisms. - Source: PubMed
Publication date: 2026/06/11
Liao WanchengYin RuiZuo FanLi YangkunDeng JiaoLi YanqiLi XiaolanTao DedingLuo XuelaiJi WeikeQin Jichao