ACACB
- Known as:
- ACACB
- Catalog number:
- Y213766
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACACB
Related genes to: ACACB
- Gene:
- ACACB NIH gene
- Name:
- acetyl-CoA carboxylase beta
- Previous symbol:
- -
- Synonyms:
- HACC275, ACC2, ACCB
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-18
- Date modifiied:
- 2016-10-05
Related products to: ACACB
Related articles to: ACACB
- Alzheimer's disease (AD) is the leading cause of dementia worldwide, yet effective therapies for this neurodegenerative disorder remain scarce. , a herb with a history of thousands of years in traditional Chinese medicine, exhibits diverse biological activities and holds potential therapeutic effects against Alzheimer's disease. However, studies on its modern pharmacological mechanisms remain relatively limited. - Source: PubMed
Publication date: 2026/04/20
Gao JieSong Ming LangLiu JieJiang ZhiBinLi WenChen YunZhi - Compared with commercial laying hens, indigenous chicken breeds generally exhibit lower reproductive performance. This study aims to elucidate the impact of abdominal fat deposition on the reproductive performance of indigenous chickens, providing a theoretical basis for the breeding of high-yielding chickens. - Source: PubMed
Publication date: 2026/04/28
Yu HailiangWu LeiWang HaoYuan ChenxuShi JiajiaJi QianyunBai YaruZhu XiaoliGuo LipingZhang ChengChen Xingyong - Cardiomyocytes primarily rely on fatty acid oxidation (FAO), which provides more than 70% of their energy. However, excessive FAO can disrupt cardiac metabolism by increasing oxygen demand and suppressing glucose utilization through the Randle cycle. Although inhibition of FAO has been investigated in heart failure, its overall therapeutic impact remains uncertain. To determine the consequences of enhanced FAO, we generated cardiomyocyte-specific ACC1 and ACC2 double-knockout (ACC dHKO) mice, which exhibit constitutively elevated FAO. ACC dHKO mice developed dilated cardiomyopathy and heart failure. Lipidomic analysis revealed marked depletion of cardiolipin caused by reduced linoleic acid, a direct consequence of excessive FAO. This cardiolipin deficiency impaired mitochondrial electron transport chain (ETC) activity, leading to mitochondrial dysfunction. Pharmacologic inhibition of FAO with etomoxir or oxfenicine restored cardiolipin levels, normalized ETC activity, and prevented cardiac dysfunction in ACC dHKO mice. These findings demonstrate that unrestrained FAO disrupts both lipid and energy homeostasis, culminating in heart failure in this model. Collectively, these results indicate that although FAO is essential for cardiac energy production, therapeutic strategies aimed at stimulating cardiac FAO may be detrimental rather than beneficial in heart failure. - Source: PubMed
Publication date: 2026/05/01
Kim Chai-WanVale GoncaloFu XiaorongMcDonald Jeffrey GDai ChongshanLi ChaoWang Zhao VSharma GauravKhemtong ChalermchaiMalloy Craig RDeja StanislawBurgess Shawn CMitsche Matthew AHorton Jay D - Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Emerging evidence indicates that fatty acid oxidation is impaired in both patients with AD and AD animal models. In the brain, fatty acid metabolism occurs predominantly in astrocytes. Diets enriched in monounsaturated fatty acids (MUFAs) are often recommended for individuals with AD. Oleic acid (OA), a common dietary MUFA, has been shown to reduce amyloid plaque accumulation in transgenic mouse models of AD. Moreover, OA decreases the expression of acetyl-CoA carboxylase beta (ACACB/ACC2), a key regulator of fatty acid β-oxidation. However, the precise mechanism by which OA may alleviate amyloid plaque deposition through modulation of brain fatty acid metabolism remains unclear. - Source: PubMed
Publication date: 2026/04/15
Xie YiBoTian JiananLi HuiPeng YahuiLi MingjieWu Yun - Egg weight (EW) is a key trait in both breeding and production for poultry. Although Zi geese demonstrate good egg-laying performance, they have relatively low EW. Identifying candidate genes and pathways associated with EW in geese is essential for enhancing genetic progress. In this study, 260 female Zi geese at 30 weeks of age were monitored individually for egg number (EN) and EW. Thirty geese, showing no significant differences in body weight and EN but significant variation in EW (P < 0.05), were selected and divided into a high egg weight (HEW) group (n = 15) and a low egg weight (LEW) group (n = 15). Egg quality traits were evaluated for both groups. From each group, six geese were randomly selected for serum biochemical profiling and untargeted metabolomics; four of these were further analyzed for transcriptomic data from the liver, ovary, and oviduct magnum. The results showed significant differences in albumen weight, yolk weight, and shell weight between HEW and LEW (P < 0.01). Serum biochemical analysis revealed higher levels of total cholesterol, triglycerides, estradiol, very low-density lipoprotein, and vitellogenin in the HEW group (P < 0.05). Transcriptomic analysis identified 278 differentially expressed genes (DEGs) in the liver, primarily enriched in antigen processing and presentation pathways, with ACACB, FDFT1, and HSPA2 highlighted as candidate genes. In the ovary, 18 DEGs were identified, with RBP1 as the key gene. In the oviduct magnum, 1,605 DEGs were enriched in protein processing in the endoplasmic reticulum, with HSPA8, HSP90AA1, and ST3GAL4 identified as candidate genes. Serum metabolomics revealed metabolites associated with EW, including cholesterol sulfate, l-tryptophan, indoxyl sulfate, and LysoPC(20:5(5Z,8Z,11Z,14Z,17Z)/0:0). Integrated multi-omics analysis identified ACSL5-LysoPC(20:5(5Z,8Z,11Z,14Z,17Z)/0:0) and ACSL5-L-tryptophan as key gene-metabolite pairs potentially regulating EW. These findings provide a theoretical foundation for understanding the genetic mechanisms underlying EW regulation in geese. - Source: PubMed
Publication date: 2026/03/21
Cong KexinLiu YunuoWang HechuanJiang KeYin JiaxinMiao XinyiYang WeiranXiao XiangChen ZhifengLiu Shengjun