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)
- Liposarcoma (LPS) is a common soft tissue sarcoma; however, its molecular pathogenesis and immune cell infiltration remain poorly understood. This study investigated potential driver genes and pathways in LPS and characterized immune cell infiltration patterns to identify potential markers for targeted therapy. Differentially expressed genes (DEGs) in LPS were analyzed by GO and KEGG pathway enrichment analysis. A protein-protein interaction network was constructed using the STRING database and visualized with Cytoscape. mRNA expression of genes with high |logFC| values was verified by RT-qPCR. Immune cell subsets were quantified using CIBERSORT. GO and KEGG analysis revealed significant functional clusters and pathways, and most verified genes were consistent with the bioinformatics analysis. Survival analysis showed that high expression of TYMS, KIF20A, BUB1B, LMNB1, RRM2, ZWINT, and RACGAP1 was significantly associated with poor overall survival and poor disease-free survival (DFS). High levels of TMSB15A, TPX2, PKM2, and PTTG1 were significantly associated with poor DFS alone. CIBERSORT analysis identified a significantly higher fraction of resting mast cells (MCs) in LPS tissues compared to normal fatty tissues (P < 0.05). TOP2A, IL-6, PCNA, CDK1, JUN, MYC, CCNB1, EGFR, ACACB, and BIRC5 were identified as potential diagnostic biomarkers of LPS, providing strong evidence for hub gene studies. Immune cell infiltration analysis further suggested that resting MCs may play a potential role in LPS development, although further experimental validation is warranted. Collectively, these findings clarify the molecular basis of LPS and provide a foundation for future research into its treatment. - Source: PubMed
Publication date: 2026/09/11
Liu ChunxiaoWang YanhuaLiu QiuxiaZhang Sha - Alzheimer's disease (AD), a neurodegenerative condition marked by amyloid-beta plaques and tau protein neurofibrillary tangles, progresses against a backdrop of essential biological processes. Manganese, an indispensable trace element for vital functions including energy metabolism and antioxidant defense, is integral to neurological health. Its precise metabolic role throughout the course of AD pathogenesis is not fully elucidated. Four essential manganese metabolism-related genes were identified as diagnostic markers through a multi-omic framework. This approach integrated Weighted Gene Co-Expression Network Analysis with machine learning ensembles (Least Absolute Shrinkage and Selection Operator/Random Forest/Extreme Gradient Boosting), followed by rigorous testing in an independent dataset. Beyond identification, we utilized CIBERSORT and ssGSEA to characterize immune infiltration and leveraged GSEA/GO/KEGG for pathway elucidation. Finally, AD patients were stratified into molecular subgroups based on these hub genes, and their underlying regulatory networks involving miRNAs and transcription factors were reconstructed. An integrated bioinformatics framework identified 12 differentially expressed genes related to manganese metabolism in AD. Machine-learning-based feature selection further pinpointed four key diagnostic biomarkers (TSPO, PTBP1, GLO1, and ACACB) with high discriminative power (AUC: 0.831-0.905). Immune infiltration analysis revealed substantial immune remodeling in AD, including an elevation of naïve B cells. Moreover, AD samples were classified into two molecular subtypes displaying distinct immune and metabolic characteristics, and regulatory miRNA/TF interaction networks were constructed for the core genes. Our results shed new light on the molecular mechanisms underlying AD and support future efforts toward early diagnosis and personalized therapeutic interventions based on molecular subtypes. - Source: PubMed
Shu ShengnanHu JiahaoHu ShanshanYao Yefeng - 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