ABCG1
- Known as:
- ABCG1
- Catalog number:
- 000933A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCG1
Related genes to: ABCG1
- Gene:
- ABCG1 NIH gene
- Name:
- ATP binding cassette subfamily G member 1
- Previous symbol:
- -
- Synonyms:
- ABC8
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2015-11-13
Related products to: ABCG1
Related articles to: ABCG1
- Clear cell renal cell carcinoma (ccRCC) is one of the most prevalent solid tumors characterized by lipid metabolic reprogramming, with extensive lipid droplet accumulation in tumor cells as a hallmark feature. Traditionally, this phenotypic trait is attributed to enhanced fatty acid synthesis, increased triglyceride (TG) storage, and impaired β-oxidation. However, emerging transcriptomic and lipidomic evidence suggests that cholesterol metabolism is also profoundly reprogrammed in ccRCC, particularly via increased reliance on high-density lipoprotein (HDL)-derived cholesterol. The classical fatty acid-TG pathway and the HDL-cholesterol axis are metabolically linked through shared substrates, collectively shaping lipid homeostasis in ccRCC. In this review, we summarize recent advances in ccRCC lipid metabolic reprogramming, with a focus on HDL-related cholesterol metabolism. We discuss the mechanisms involving von Hippel-Lindau (VHL) loss and hypoxia-inducible factor (HIF) activation, including SCARB1-mediated cholesterol uptake, LXRα-ABCA1/ABCG1-dependent cholesterol efflux, and SOAT1-driven re-esterification of free cholesterol into cholesteryl esters (CE). Furthermore, we outline potential therapeutic targets within these pathways and highlight critical knowledge gaps that merit further investigation. This review provides a conceptual framework for understanding HDL-centered cholesterol metabolism in ccRCC and highlights potential metabolic vulnerabilities for therapeutic targeting. - Source: PubMed
Publication date: 2026/09/01
Wu LizeXue HuayingWu YifeiShen NingningYang ZhiqingGao LifangMa WenxiaWang Chen - Very-low-density lipoprotein cholesterol (VLDL-C) may contribute to cardiometabolic multimorbidity (CMM), but prospective evidence on cumulative exposure and cellular evidence in established foam cells remain limited. We aimed to evaluate the association between cumulative estimated VLDL-C exposure and incident CMM and to explore VLDL-r elated changes in established foam cells. - Source: PubMed
Wang Lu-ZhaoCui Kai-JunWang Xin-MengJia Run-KunXie Xin - Pancreatic β cells require tightly controlled cholesterol distribution to maintain glucose sensing, insulin-granule trafficking, and regulated exocytosis. ATP-binding cassette transporter A1 (ABCA1) exports cellular cholesterol and phospholipids to lipid-poor apolipoprotein A-I and is a central component of β-cell cholesterol homeostasis. β-cell-specific Abca1 deletion causes cholesterol accumulation and impaired glucose-stimulated insulin secretion, whereas human studies of rare ABCA1 loss-of-function mutations have reported heterogeneous secretory phenotypes. Endocrine, metabolic, inflammatory, lipoprotein, and post-transcriptional signals regulate pancreatic ABCA1. Exendin-4 activates CaMKK/CaMKIV/PREB-dependent transcription, insulin-like growth factor-1 acts through PI3K/Akt/FoxO1 signaling, and pemafibrate increases ABCA1 through PPAR-α-dependent regulation in experimental models. Conversely, angiotensin II, tumor necrosis factor-α, oxidized low-density lipoprotein, and -methyl-D-aspartate suppress ABCA1 through distinct or partially convergent pathways, while miR-33a directly suppresses ABCA1 in human and mouse islets. β-cell function depends on the balance among LDLR-dependent cholesterol uptake, PCSK9-mediated receptor regulation, intracellular sterol trafficking and esterification, ABCG1-dependent handling, and ABCA1-dependent export rather than on total cellular cholesterol alone. Although several regulator-specific mechanisms remain preclinical and await independent replication, this review integrates these pathways and discusses their nutritional and translational relevance in type 2 diabetes. - Source: PubMed
Publication date: 2026/09/02
Fukunaga KensakuKobayashi ToshihiroSaheki TakanobuYoshimura TakafumiJiang WenyiZhang HaotianLy RathanaKumano MarinoYamashita AyakoImachi HitomiMurao Koji - Host metabolic reprogramming is increasingly recognized as a determinant of viral pathogenesis, yet its role in genetic disease resistance remains elusive. This study investigated the survival and lipid metabolic dynamics of Pekin duck combinations-pure resistant (RR), pure susceptible (SS), and reciprocal crosses (RS: R♀ × S♂; SR: S♀ × R♂)-following DHAV-3 infection. Phenotypic analysis revealed striking maternal inheritance in disease resistance: RS females exhibited the lowest mortality (22.7%), significantly outperforming SR females (51.4%) and even the resistant RR pure line (27.0%). To uncover the underlying mechanisms, we analyzed pre- and post-infection lipid profiles. Pre-infection liver biochemistry identified baseline cholesterol (CHOL) and LDL-C as robust predictors of viral susceptibility, with the highly susceptible SS group exhibiting the highest levels. Following viral challenge, plasma lipid dynamics and liver function indicators (ALT, AST) fluctuated significantly depending on cross-combination, sex, and time. Furthermore, the dynamic expression of key lipid metabolism genes, particularly cholesterol efflux regulators (ABCA1, ABCG1), was tightly orchestrated by genetic background and sex interactions. Overall, these findings demonstrate that baseline lipid profiles and post-infection lipid network reshuffling dictate the disease resistance differences among hybrid combinations. The exceptional resistance of the RS combination highlights the critical role of maternal effects and offers a metabolic perspective for strategic crossbreeding in poultry. - Source: PubMed
Publication date: 2026/07/27
Liang SuyunZhang MeijuanLi HuihuiLi BingMao MingtianLuo DaewiGuo ZhanbaoTang YiHou Shuisheng - Indoxyl sulfate (IS) is a protein-bound uremic toxin that accumulates in patients with chronic kidney disease (CKD) and promotes oxidative stress, endothelial dysfunction, vascular smooth muscle cell proliferation, and fibrosis, thereby contributing to vascular stenosis in patients receiving hemodialysis. CKD is also commonly associated with vitamin D deficiency, which is linked to vascular calcification, immune dysregulation, and inflammation. This study aims to investigate the preventive effects of 1,25(OH)2D3 (active vitamin D) against IS-induced macrophage inflammatory activation and cholesterol dysregulation. Macrophages were pretreated with 30 nM 1,25(OH)2D3 for 12 and 24 h, followed by exposure to IS at concentrations of 125 and 250 µg/mL for 24 h. Morphological changes were observed under a microscope. To assess macrophage phenotype-associated changes, qPCR was performed to analyze the expression of M1-like/pro-inflammatory markers (TNF-α and IL-1β) and M2-like/anti-inflammatory phenotype-associated markers (CD163 TGF-β and IL-10). Cholesterol metabolism was assessed using a cholesterol efflux assay, qPCR analysis of ABCA1 and ABCG1 and Oil Red O staining for intracellular lipid accumulation. Protein expression of inflammatory mediators, TGF-β1, and cholesterol efflux transporters was further evaluated by western blotting. 1,25(OH)2D3 pretreatment modulated IS-associated inflammatory responses, as reflected by changes in selected M1-like/pro-inflammatory mediators, including iNOS, IL-6 and IL-1β. Conversely, 1,25(OH)2D3 increased selected M2-like/anti-inflammatory phenotype-associated markers, including CD163 and IL-10. Furthermore, 1,25(OH)2D3 pretreatment preserved cholesterol efflux capacity and modulated ABCA1 and ABCG1 expression in a time- and transporter-dependent manner, accompanied by reduced intracellular lipid accumulation as shown by Oil red O staining. These findings suggest that 1,25(OH)2D3 may protect macrophages against IS-induced inflammatory activation and cholesterol dysregulation, highlighting its potential as a preventive or modulatory approach for macrophage-mediated vascular dysfunction in CKD. - Source: PubMed
Publication date: 2026/09/11
Kong Kyoung HyeYang KyungwonRyu Jung-Hwa