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
- This study aimed to characterize the genomic diversity, population structure, and candidate regions consistent with selection in Hamdani (HAM) sheep using high-density SNP generated by double-digest restriction site-associated DNA sequencing (ddRADseq). A total of 20 animals were sampled, and after quality filtering, 310,663 SNPs from 18 individuals were retained for downstream analyses. Genetic diversity parameters indicated a relatively high level of genomic variation within the breed ( = 0.323 ± 0.01 and = 0.326 ± 0.01) and low levels of inbreeding ( = 0.029 ± 0.02 and = 0.008 ± 0.01), suggesting that the population has maintained substantial genetic diversity and has not experienced recent intensive inbreeding. Population structure analyses revealed that HAM sheep form a distinct genetic cluster separated from Turkish fat-tailed breeds, reflecting their unique genetic background and breeding history. Footprints of selection analyses based on runs of homozygosity (ROH) and integrated haplotype score (iHS) identified preliminary candidate genomic regions consistent with selection. After FDR correction, 12 of the 34 trait-chromosome combinations tested for the iHS-derived regions and three of the eight combinations tested for the ROH-derived regions were significantly enriched. Functional annotation highlighted biologically relevant candidate genes involved in reproductive performance (, , and ), lipid metabolism ( and ), and environmental adaptation ( and ). This ddRADseq-based genome-wide characterization provides preliminary information on genetic variability and candidate genomic regions consistent with selection in HAM sheep. Therefore, further studies focusing on a larger sampling strategy across multiple different sheep breeds are needed to design conservation, breeding, and future genomic selection programs. - Source: PubMed
Publication date: 2026/09/16
Demir EbruPerini FrancescoDemir EymenLasagna EmilianoBilginer ÜmitKaya SarpGöneci Fidan BesteAlkan SezaiKarslı TakiKarslı Bahar Argun - Macrophages and microglia serve as both "scavengers" and "immune sentinels" to maintain tissue homeostasis. However, when the lipid load exceeds their processing capacity, these cells transform into foam cells, thereby driving chronic inflammation and impairing tissue repair. Despite their distinct organ systems, atherosclerosis (AS) and spinal cord injury (SCI) converge on a common pathological cascade-foam cell formation-characterized by "enhanced lipid uptake, impaired cholesterol efflux, disrupted lysosomal/autophagic processing, and ER stress/ROS/NLRP3-mediated inflammatory amplification." This review systematically dissects and compares the molecular mechanisms underlying macrophage foaming in AS and SCI, with a particular focus on the similarities and differences in ABCA1/ABCG1-mediated cholesterol efflux, lipid droplet autophagy, the ER stress-NLRP3 axis, and nuclear receptor regulatory networks. Furthermore, it explores therapeutic avenues that target lipid metabolic reprogramming, including natural products, biomimetic nanomedicines, and genetic interventions. By establishing a cross-disease framework for lipid homeostasis disruption, this paper challenges traditional organ-centric views and provides a theoretical foundation that may accelerate the development of shared therapeutic strategies for AS and SCI. - Source: PubMed
Publication date: 2026/09/21
Tan GuinaWang XiaoxinChen JingFeng RuChu HongyuYang DegangLi JunYang MingliangLi JianjunHuang YingGao Feng - Dendritic cell (DC)-based immunotherapy shows limited efficacy against hepatic fibrosis, and the underlying mechanometabolic crosstalk remains unclear. Here, from a mechanobiological perspective, we demonstrate that increased extracellular matrix (ECM) stiffness in the fibrotic liver triggeres antigen-independent abnormal DC maturation, characterized by elevated co-stimulatory molecules, impaired phagocytic capacity, reduced IL-10 secretion, and suppressed regulatory T cell (T) differentiation. Mechanistically, the stiff ECM inhibites the AMPK-LXRα-ABCG1 signaling axis in DCs, reducing cholesterol efflux and promoting intracellular cholesterol accumulation. Cholesterol depletion or AMPK activation reverses stiffness-induced abnormal DC maturation. In mouse models, combined treatment with pirfenidone and simvastatin reduced liver stiffness and collagen deposition, and restored immune tolerance by correcting DC cholesterol metabolism. Our study identifies a mechanometabolic pathway linking matrix stiffness to DC dysfunction, providing a promising immunometabolic strategy for antifibrotic therapy. - Source: PubMed
Publication date: 2026/09/01
Zeng XianlinLuo PanWu CuifangLong JinhuaZhang ShuaiWang YunTeng LijingZhang HonghongFan DeqiaoHu ZuquanXu PuZeng Zhu - N6‑methyladenosine (m6A), the predominant internal modification in eukaryotic mRNAs, has emerged as a significant epigenetic regulator in atherosclerosis; however, its precise mechanistic contributions remain inadequately elucidated. The present study demonstrated that the m6A demethylase fat mass and obesity‑associated (FTO) regulates autophagy, lipid metabolism and plaque vulnerability by targeting autophagy related 5 (ATG5). FTO knockdown resulted in reduced ATG5 expression, thereby suppressing autophagy and downregulating ATP‑binding cassette transporter A1 (ABCA1) and ATP‑binding cassette sub‑family G member 1 (ABCG1). The regulation of ATG5 expression by FTO occurs through direct binding to its transcripts as well as m6A‑mediated mechanisms. Increased m6A modification on ATG5 mRNA following FTO silencing enhanced its recognition by YTH domain‑containing family 1, leading to transcript degradation and diminished protein levels. Consequently, autophagy and cholesterol efflux pathways were inhibited. experiments revealed that specific FTO knockdown compromised plaque stability and impaired ATG5‑mediated autophagy, in addition to downregulating ABCA1 and ABCG1. These findings highlighted the FTO‑ATG5‑ABCA1/ABCG1 axis as a critical regulator of autophagy and lipid homeostasis in atherosclerosis. - Source: PubMed
Publication date: 2026/09/18
Guo FengxiaHe MeiLi YaonanZhu KangningHu Bing - 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