ACACB (Human) Recombinant Protein (Q01)
- Known as:
- ACACB (Human) Recombinant Protein (Q01)
- Catalog number:
- H00000032-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ACACB (Human) Recombinant Protein (Q01)
Related genes to: ACACB (Human) Recombinant Protein (Q01)
- 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 (Human) Recombinant Protein (Q01)
Related articles to: ACACB (Human) Recombinant Protein (Q01)
- 1. The following study investigated the regulation of Intramuscular fat (IMF) deposition at different developmental stages in Jingyuan chickens. Pectoral muscles from hens at 42, 126 and 180 days of age were analysed using transcriptome sequencing and weighted gene co‑expression network analysis (WGCNA).2. A total of 1187, 1377 and 617 differentially expressed genes (DEGs) were identified in the three pairwise comparisons, respectively. Among these, , and are known to be involved in IMF synthesis and metabolism through energy and amino acid metabolic pathways.3. The WGCNA data identified three modules (MEyellow, MEbrown, MEdarkred) that were significantly correlated with IMF content and age ( < 0.05). Functional analysis indicated that , and were enriched in both FoxO and GnRH signalling pathways. This suggested potential roles in IMF deposition. Further investigation of DEG and the three modules revealed and as candidate genes that could influence IMF deposition in muscle.4. The data represents a transcriptomic resource for IMF deposition in Jingyuan chicken breast muscle. The results identified candidate genes for future molecular breeding aimed at improving meat quality. - Source: PubMed
Publication date: 2026/07/03
Wang HWang CZhao WYu BHu JZhang JGu Y - Liver function is impaired in metabolic dysfunction-associated fatty liver disease. Previous studies have demonstrated that oxygen availability in the tissue microenvironment affects adipose tissue and skeletal muscle function, but its hepatic effects remain unclear. This study aimed to investigate the impact of oxygen levels on metabolic pathways in HepG2 cells. Nonlipid-loaded and lipid-loaded HepG2 cells were exposed to different physiological O levels (5% and 10%) or standard laboratory conditions (21% O) for 24 h. Thereafter, we determined lipid content, gene expression of metabolic markers, glycogen content, and glucose release. Furthermore, mitochondrial respiration and glycolytic activity were assessed by measuring the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), respectively. Exposure to 5% O increased the expression of the gluconeogenic gene glucose-6-phosphatase catalytic subunit 1 () in both nonlipid-loaded and steatotic HepG2 cells compared with 21% O ( < 0.001). Furthermore, 5% O decreased the expression of lipogenic genes [sterol regulatory element binding transcription factor 1 (), acetyl-CoA carboxylase beta (), and fatty acid synthase ()] in nonlipid-loaded and/or steatotic cells (all < 0.05), whereas genes involved in fatty acid oxidation [peroxisome proliferator-activated receptor gamma coactivator 1-alpha (), < 0.001 and peroxisome proliferator-activated receptor alpha (), = 0.038] were downregulated in steatotic cells. Low oxygen exposure increased glycogen content in nonlipid-loaded and steatotic cells (both < 0.001) and reduced glucose release ( < 0.05). Finally, low oxygen exposure reduced OCR ( < 0.05) and increased glycolysis ( < 0.001) in both nonlipid-loaded and steatotic cells compared with 21%. In conclusion, our findings demonstrate that reduced oxygen availability in the microenvironment has marked effects on metabolic pathways in nonlipid-loaded and steatotic hepatocytes, inducing a metabolic shift to enhanced reliance on glucose as an energy source. Oxygen availability in the tissue microenvironment affects adipose tissue and skeletal muscle function, but the effects of oxygen levels on hepatic metabolism are unclear. Low oxygen exposure altered expression of genes involved in glucose and lipid metabolism, increased glycogen content, decreased glucose release and oxygen consumption, and increased glycolytic rate compared with exposure to 21% O in both nonlipid-loaded and steatotic HepG2 cells, indicative of a shift to enhanced reliance on glucose as an energy source. - Source: PubMed
Publication date: 2026/07/02
Li GengDubois Ludwig JBiemans RianneGoossens Gijs HMeex Ruth C R - Lipid storage myopathy (LSM) is characterized by abnormal lipid accumulation in skeletal muscle. Emerging evidence suggests that environmental factors, including the use of antidepressants such as sertraline, may trigger LSM. Given the established link between hyperhomocysteinemia (HHcy) and disrupted lipid metabolism, we investigated its potential role in skeletal muscle lipid deposition. - Source: PubMed
Publication date: 2026/06/16
Su MenghanJiao JiaqiZhao JunsenMa JingZhang HuiqiuLiu QiyunWang JuanLiu DanWen QiWang JianliChang XueliGuo JunhongZhang Wei - The hybrid golden pompano "Chenhai No. 1" (CH), generated through distant hybridization [(♀ × ♂ ) × ♂ ], exhibits significantly enhanced growth performance compared to its parental (TO). To elucidate the molecular mechanisms underlying this rapid growth, we performed integrated transcriptomic and untargeted metabolomic profiling of muscle tissue. Transcriptomic analysis identified 3172 differentially expressed genes (DEGs), with weighted gene co-expression network analysis (WGCNA) highlighting the 'darkorange2' module as strongly associated with rapid growth. Key DEGs, including , , and , were upregulated and implicated in energy metabolism, glycolysis, and signal transduction. Metabolomic profiling detected 576 significantly altered metabolites, predominantly enriched in glycolysis, the tricarboxylic acid (TCA) cycle, amino acid metabolism, lipid biosynthesis, and mTOR signaling. Integrated analysis revealed coordinated alterations between core module genes and differential metabolites in interrelated pathways, including correlations between / and glyceraldehyde-3-phosphate, and phosphatidylcholine/phosphatidylethanolamine, and and leucine. These findings suggest that the growth advantage of CH arises from the coordinated enhancement of energy metabolism, amino acid sensing, and lipid metabolic remodeling, establishing a synergistic transcription-metabolism regulatory network. This study provides multi-omics insights into the molecular basis of rapid growth in an economically important teleost fish. - Source: PubMed
Publication date: 2026/06/18
Liang HongxuanGao XinChen ZhennianQin LangXu CanYang YingyingWang YuxiangHu FangzhouHuang XuWu ChangLiu Shaojun - Egg-laying performance varies significantly among different chicken breeds. The liver, as the central organ responsible for yolk precursor synthesis, largely determines the egg production performance of poultry. However, the underlying genetic basis of these phenotypic differences remains poorly understood. In this study, we systematically compared the transcriptomic differences and dynamic changes in three-dimensional (3D) genome organization in the livers of a high-producing commercial breed (White Leghorn) and a low-producing indigenous breed (Wenchang chicken) during the laying period. Transcriptomic analysis revealed that significantly upregulated genes in White Leghorns were highly enriched in lipid metabolism-related pathways, including CPT1A, ACSL1, ACACB, ACOX1, EHHADH, DHCR7, and SQLE, whereas highly expressed genes in Wenchang chickens were mainly enriched in pathways such as the ribosome. 3D genomic analysis demonstrated that although the global chromatin framework of the liver was relatively conserved between the two breeds, significant breed-specific remodeling occurred in local spatial organization. At the compartment level, key metabolic genes such as BBOX1 and GRB14 underwent B-to-A compartment switching and transcriptional activation in White Leghorns, which may be associated with their high laying trait. At the topologically associating domain (TAD) level, the livers of White Leghorns exhibited relatively weaker boundary insulation and a looser intra-domain folding state. Furthermore, the functional enrichment results of breed-specific TAD boundary genes were relatively consistent with the transcriptomic profiles. At the chromatin loop level, White Leghorns displayed stronger intra-loop spatial interactions. Critically, White Leghorn-specific chromatin loops precisely anchored and upregulated some key genes involved in lipid metabolism, such as ACSL1, ACOX1, and EHHADH, whereas Wenchang chicken-specific loops primarily drove the expression of ribosome-related genes. In summary, this study reveals a close correlation between the dynamic changes in the 3D chromatin structure and the transcription differences in the livers of the two chicken breeds, and these differences may be linked to egg production performance. These findings provide new insights into the genetic basis underlying the liver's role in regulating poultry laying performance. - Source: PubMed
Publication date: 2026/06/10
Wang ShenaoCao YuediTian Geng G