ABCG2
- Known as:
- ABCG2
- Catalog number:
- 000934A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCG2
Related genes to: ABCG2
- Gene:
- ABCG2 NIH gene
- Name:
- ATP binding cassette subfamily G member 2 (Junior blood group)
- Previous symbol:
- -
- Synonyms:
- EST157481, MXR, BCRP, ABCP, CD338
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
Related products to: ABCG2
Related articles to: ABCG2
- Population-frequency evidence is indispensable for planning pharmacogenomic services, but broad ancestry categories do not reliably capture the distribution of clinically important alleles, haplotypes, and structural variants. We undertook a systematic synthesis of pharmacogenetic variation reported in Vietnamese populations and evaluated its relevance to clinical implementation. - Source: PubMed
Publication date: 2026/09/03
Hoang Van Thi BichTran Anh VanBui Tham ThiVu Quynh ThiNgo Mai Thi QuynhNguyen Khai VanNguyen Phuong Thi Thu - Hyperuricemia, caused by purine metabolism dysfunction and impaired uric acid excretion, is increasing in prevalence globally. Current urate-lowering drugs have limitations in safety and applicability. The gut, which is central to uric acid production and excretion, hosts microbiota closely linked to uric acid metabolism and gout-related inflammation. This paper summarizes advances from PubMed and CNKI (2012-March 2026) on microbiota-mediated regulation of uric acid metabolism and gout. Gut microbiota promote hyperuricemia and gout multiple mechanisms: regulating purine metabolism and uric acid production, degrading urate, modulating intestinal urate transport, and activating inflammatory pathways. We further classify microbiota-targeted urate-lowering interventions into four categories: (i) microbial metabolites and functional strains, (ii) microbiota-modulating natural products, (iii) microbiota-utilizing polysaccharides, and (iv) bioactive peptides. These strategies have unique advantages including high intestinal exposure, microbiota responsiveness, structural diversity, and multi-pathway regulation potential, acting key axes such as microbiota-PPARγ-ABCG2 and TLR4/NF-κB-NLRP3. By targeting systemic regulation instead of simple transporter inhibition, they fill critical gaps in current therapy. From a medicinal chemistry perspective, these molecules are promising prototype templates for safer, more effective anti-hyperuricemic and anti-gout drugs. - Source: PubMed
Publication date: 2026/09/01
Jiang YuxinShi XiaoyuYang QianPang JianxinZhan PengXu ShujingWu Ting - The aim of this study was to evaluate the expression levels of ABCG2 and ABCC2, members of the ATP-binding cassette (ABC) transporter gene family, in patients with acute pancreatitis and to investigate their potential associations with disease presence as well as clinical and radiological disease severity. This prospective study included 80 patients diagnosed with acute pancreatitis and 96 healthy controls. Disease severity in acute pancreatitis was assessed using the Ranson score and computed tomography (CT) findings. ABCG2 and ABCC2 gene expression levels were measured in peripheral blood samples using quantitative real-time polymerase chain reaction (qRT-PCR). Statistical analyses, including between-group comparisons and evaluations of associations between gene expression and disease severity, were performed using SPSS version 25.0. ABCG2 gene expression levels were significantly lower in patients with acute pancreatitis than in healthy controls (p = 0.025). However, ABCG2 expression was significantly higher in moderate and severe acute pancreatitis cases based on CT findings compared with mild cases (p = 0.038). ABCC2 gene expression showed no significant association with either the presence of acute pancreatitis or disease severity. In ROC analysis, the area under the curve (AUC) for ABCG2 gene expression was statistically significant (AUC = 0.598, p = 0.025). This study suggests that ABCG2 gene expression may be associated with the presence of acute pancreatitis and radiological disease severity. ABCG2 may represent a dynamically regulated candidate biomarker related to inflammatory and cellular stress processes in acute pancreatitis. Further studies including larger patient cohorts and preferably multicenter designs are needed to validate these findings. - Source: PubMed
Baş SüleymanGüzel Tanoğlu EsraTanoğlu AlpaslanKarahan Hafize TuğbaGökçe Muhammed SaidYeniçeri MuratŞenoymak Mustafa CanArslan Kadem - 5-Aminolevulinic acid (ALA) is administered as a prodrug for tumor fluorescence detection and photodynamic therapy (PDT) after being converted endogenously to the active drug protoporphyrin IX (PpIX). As a substrate of the ABCG2 transporter, PpIX is subject to outward transport in cells with ABCG2 expression, resulting in reduced PpIX fluorescence and PDT effect. Due to the lack of approved ABCG2 inhibitors, lapatinib (Lap), a kinase inhibitor approved for cancer treatment, has been repurposed as an ABCG2 inhibitor for the enhancement of ALA. To provide evidence that Lap enhances ALA by inhibiting ABCG2, we knocked down ABCG2 in four tumor cell lines and evaluated the effects of Lap on enhancing ALA-PpIX fluorescence and PDT in the wild-type and ABCG2-knockdown cell lines. ABCG2 knockdown enhanced ALA-PpIX fluorescence and PDT response, underscoring the importance of ABCG2 in regulating intracellular PpIX accumulation. However, compared with the corresponding wild-type cell lines, Lap induced less enhancement of PpIX fluorescence and PDT in ABCG2-knockdown cell lines, particularly at high concentrations and in cell lines with low ABCG2 activities. By downregulating ABCG2 in tumor cells, we showed that Lap-induced ALA enhancement was reduced, demonstrating that Lap enhances ALA by blocking ABCG2-mediated PpIX efflux. - Source: PubMed
Publication date: 2026/09/16
Wescoat JordynCabral CorinnaChen Bin - Uric acid transporters mediate renal and extrarenal urate handling and may contribute to blood pressure (BP) regulation. This study examined the associations of common single-nucleotide polymorphisms (SNPs) in key urate transporter genes (SLC2A9, ABCG2, SLC17A3, SLC22A7, SLC22A6, SLC22A11, SLC22A12, and ABCC4) with salt sensitivity, longitudinal BP changes, and incident hypertension. Data were derived from the Baoji Salt-Sensitivity Study, a family-based cohort in which 514 Chinese adults completed a controlled dietary sodium intervention and were followed prospectively for 14 years. After multivariable adjustment and multiple-testing correction, ABCG2 rs2054576 and rs4491984 were associated with DBP response to low-salt diet; SLC22A6 rs4149170 with SBP and DBP responses; ABCG2 rs12505410 and SLC22A12 rs7932775 with DBP and MAP responses; and ABCC4 rs1189466 and rs17189390 with SBP, DBP, and MAP responses. During high-salt intake, SLC2A9 rs3733591 was associated with SBP and MAP responses; and SLC22A11 rs3759053, ABCC4 rs17189390 and rs9590211 were associated with SBP, DBP, and MAP responses. Over 14 years of follow-up, SLC2A9 rs3733591 and SLC17A3 rs1165165 were associated with longitudinal systolic BP (SBP) change; ABCG2 rs2054576, SLC22A7 rs2270860, SLC22A12 rs79226484, and ABCC4 rs1189466 were associated with diastolic BP (DBP) and MAP change; and SLC22A6 rs4149170 and ABCC4 rs9590220 and rs7322318 were associated with change in SBP, DBP and MAP. Additionally, ABCC4 rs7982809 and rs869951 were associated with incident hypertension over the 14-year follow-up. These findings suggest that genetic variation in urate transporters may contribute to salt sensitivity, long-term BP progression, and hypertension risk, supporting a possible role for urate-transport pathways in BP regulation. - Source: PubMed
Chang Ming-KeKong Ling-YunZhang Zhuo-RanYao ShiWang XinLi HaoWang YangGao Wei-Hua