Polyclonal Rabbit ACAD10 Antibody
- Known as:
- Polyclonal Rabbit ACAD10 Antibody
- Catalog number:
- KA0064
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ACAD10 Antibody
Related genes to: Polyclonal Rabbit ACAD10 Antibody
- Gene:
- ACAD10 NIH gene
- Name:
- acyl-CoA dehydrogenase family member 10
- Previous symbol:
- -
- Synonyms:
- MGC5601
- Chromosome:
- 12q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-17
- Date modifiied:
- 2018-05-03
Related products to: Polyclonal Rabbit ACAD10 Antibody
Related articles to: Polyclonal Rabbit ACAD10 Antibody
- Acute myocardial infarction (AMI) caused by thrombosis is a major cause of mortality. A polymorphism in gene (rs671) is found in approximately 30% to 50% of East Asians, and it is a risk factor for AMI. This mutation impairs aldehyde dehydrogenase 2 (ALDH2) function, but the effect of ALDH2 on platelet activation and thrombosis is unknown. - Source: PubMed
Publication date: 2026/02/06
Sun SongZhang XuanYue HongweiFan CuiqinZhang YiGuo YunyunLi XingmingCui SumeiYang KehuiZhao XiangkaiZhang ChengPan ChangXu FengChen Yuguo - Epidemiologic and genetic associations of modifiable risk factors with stroke have been widely reported. However, the degree to which the shared genetic determinants are involved in these associations is unclear. Our study aimed to investigate the shared genetic etiology between stroke and its leading risk factors and to identify shared genomic loci, genes, and pathways that are widely distributed across the genome. - Source: PubMed
Publication date: 2025/11/15
Yang ZewenLiu HanchenZhang GuanghaoMa HongyuWang LijunLiu GuopingHuang QinghaiZhou YuYang PengfeiLiu Jianmin - This study aimed to explore potential causal relationships between mitochondria- related genes and irritable bowel syndrome (IBS) using integrative multi-omics analysis. - Source: PubMed
Publication date: 2025/10/29
Xu BeibeiZhang JiHuang YiWang XiuyanTeng MiaomiaoWeng XuejianYu YingcongZheng Endian - Telomere shortening is a well-established marker of cellular aging and genomic instability. While the relationship between leukocyte telomere length and cardiovascular diseases has long been of interest, their genetic interplay remains incompletely understood. In this study, we observe substantial genetic overlap beyond genome-wide correlations and identify a potential causal relationship between leukocyte telomere length and coronary artery disease. Specifically, we discover 248 pleiotropic loci, 22 of which show strong evidence of colocalization. Some shared loci implicate multiple pleiotropic genes across different trait pairs, including ALDH2, ACAD10, TMEM116, SH2B3 (all at 12q24.12), TMED6 (16q22.1), SERPINF1 (17p13.3), and XPO7 (8p21.3). Functional analysis highlights key pathways involved in DNA biosynthesis and telomere maintenance. Notably, SH2B3 is validated through proteome-wide Mendelian randomization analysis, suggesting its potential as a therapeutic target. Here we report the shared genetic basis between leukocyte telomere length and cardiovascular diseases, providing valuable insights into future therapeutic developments. - Source: PubMed
Publication date: 2025/09/30
Qiao JunWang QianZhao YuhuiChang MinjingSun ShuoZhang PengweiYao KaixinChen MiaoranZheng LeileiXing XiaolongCai LiuyangJegga Anil GJiang LeiPauklin SiimZou RongjunYang YiningFeng Yuliang - Fatty acid β-oxidation is a central catabolic pathway with broad health implications. However, various fatty acids, including 4-hydroxy acids (4-HAs), are largely incompatible with β-oxidation machinery before being modified. Here we reveal that two atypical acyl-CoA dehydrogenases, ACAD10 and ACAD11, drive 4-HA catabolism in mice. Unlike other ACADs, ACAD10 and ACAD11 feature kinase domains that phosphorylate the 4-hydroxy position as a requisite step in converting 4-hydroxyacyl-CoAs into conventional 2-enoyl-CoAs. Through cryo-electron microscopy and molecular modeling, we identified an atypical dehydrogenase binding pocket capable of accommodating this phosphorylated intermediate. We further show that ACAD10 is mitochondrial and necessary for catabolizing shorter-chain 4-HAs, whereas ACAD11 is peroxisomal and enables longer-chain 4-HA catabolism. Mice lacking ACAD11 accumulate 4-HAs in their plasma and females are susceptible to body weight and fat gain, concurrent with decreased adipocyte differentiation and adipokine expression. Collectively, we present that ACAD10 and ACAD11 are the primary gatekeepers of mammalian 4-HA catabolism. - Source: PubMed
Publication date: 2025/06/19
Rashan Edrees HBartlett Abigail KKhana Daven BZhang JingyingJain RaghavWade GinaAbriata Luciano ASmith Andrew JBaker Zakery NCook TaylorCaldwell AlanaChevalier Autumn RForny PatrickPfleger Brian FPeraro Matteo DalYuan PengAmador-Noguez DanielSimcox Judith APagliarini David J