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
- ABCG2-mediated drug efflux is a major cause of multidrug resistance (MDR), reducing the activity of various anticancer agents. This study evaluated the role of Golvatinib, originally developed as a c-MET/VEGFR2 inhibitor, as a potential ABCG2 modulator in ABCG2-expressing MDR cells. Golvatinib significantly restored cellular sensitivity to representative ABCG2 substrates, by inhibiting efflux of substrates and increasing intracellular drug accumulation. ABCG2 expression and membrane localization remained unchanged, indicating that this reversal was not due to downregulation or relocation of ABCG2 transporter. Cellular thermal shift analysis supported direct engagement of Golvatinib with the ABCG2 transporter, and apoptosis assay showed that the combination restored chemotherapy-induced cell death in MDR cancer cells. In addition, chemosensitization remained significant in 3D spheroid cell culture. Molecular docking with ABCG2 predicted that Golvatinib binds within the transmembrane drug-binding pocket, consistent with competitive/steric inhibition of substrate transport. These results support the rationale of Golvatinib as a candidate for combination therapy strategies targeting ABCG2-related MDR. - Source: PubMed
Publication date: 2026/08/18
Chen Xuan-YuCao Lu-QiChen XiangPatel HarshDaartey Abel BLan YanningHe XinmanWu Zhuo-XunAgarwal SaurabhStefan Sven MarcelChen Zhe-Sheng - Hyperuricemia (HUA) is a heterogeneous group of metabolic disorders caused by long-term disturbances in purine metabolism. In recent years, although adult HUA and gout have been extensively studied, the understanding of HUA and gout in children and adolescents remains insufficient. Diagnostic criteria for adult HUA are well-established, but no consensus has yet been reached regarding its definition in children and adolescents. This review summarizes the current understanding of pediatric HUA, emphasizing its genetic basis, metabolic mechanisms, and clinical associations. ATP-binding cassette subfamily G member 2 (ABCG2) dysfunction, gene-defined forms of autosomal dominant tubulointerstitial kidney disease (ADTKD), particularly ADTKD-UMOD and ADTKD-REN, and selected purine metabolism disorders contribute to early-onset HUA, gout, nephrolithiasis, and renal involvement. Obesity-related insulin resistance (IR) may promote urate accumulation through pathways linked to oxidative stress, endothelial dysfunction, and inflammasome activation. Persistent elevation of uric acid (UA) has been associated with chronic kidney disease (CKD) progression, elevated blood pressure (BP), and subclinical cardiovascular remodeling. However, many of these mechanistic associations are supported primarily by adult and experimental studies and require further validation in children. We also review non-pharmacological management and indication-based pharmacological treatment strategies for pediatric HUA. These indications include asymptomatic hyperuricemia (AH), pediatric gout, UA nephrolithiasis, inherited purine metabolism disorders, CKD-associated HUA, and tumor lysis syndrome (TLS)-associated acute HUA, with emphasis on pediatric evidence, regulatory approval, off-label use, dosing, monitoring, and safety. In children, asymptomatic serum urate elevation is often the first recognized presentation, whereas nephrolithiasis, gout, renal dysfunction, or acute HUA should prompt evaluation for genetic, metabolic, renal, or treatment-related causes. These findings underscore the need for early identification and personalized intervention in children with HUA to prevent long-term renal and metabolic complications. - Source: PubMed
Publication date: 2026/08/10
Zhou JingLv JianingHong ChunhuanLiu QinhaoJin ShuqingZhang YiLiu Yunfeng - This study investigates the isolation and expansion of limbal epithelial stem cells (LESC) and limbal mesenchymal stem cells (LMSC) from human corneal donor tissue using magnetic-activated cell sorting (MACS) with ABCG2 and CD90 microbeads, respectively. The tissue was enzymatically digested, and the resulting cell populations were characterized based on their marker expression and growth properties. A weak negative correlation between storage duration and cell yield was observed, while donor age had minimal influence. Laminin-111 coating was used to investigate its effect on cell growth and stem cell marker expression. Immunofluorescence analysis confirmed the enrichment of ABCG2 LESC and CD90 LMSCs by using magnetic-activated cell sorting (MACS). ABCG2 cells exhibited typical stem cell morphology and high expression of p63α and CK15, while LMSC showed mesenchymal characteristics, including vimentin expression. Expansion of ABCG2 LESC revealed a shift from epithelial to mesenchymal-like cells over several passages. While CD90-based MACS enables a robust and reproducible isolation of LMSC, ABCG2 alone is not sufficient for the isolation of a pure and stable LESC population. These findings highlight the need for combinatorial or sequential sorting strategies, such as CD90 followed by ABCG2, to achieve pure LESC populations. This study underscores the potential of discarded corneoscleral tissue as a valuable source for regenerative therapies and the need for optimized protocols to improve LESC isolation by MACS. - Source: PubMed
Publication date: 2026/08/21
Mueller MichelleAnischenko NicoleLemmer KatjaSzurman Peter - Hyperuricemia (HUA) is primarily attributed to insufficient uric acid (UA) excretion. 6'‑O‑Caffeoylarbutin (CA), the primary bioactive constituent of anti‑gout herbal tea (Que Zui tea), has demonstrated potential urate‑lowering effects; however, its underlying mechanisms require further elucidation. In the present study, a hypoxanthine (HX) and potassium oxonate (PO) induced hyperuricemia (HUA) mouse model was established to assess the effects of different doses of CA. Biochemical analyses, histopathological examination, western blotting and 16S rRNA gene sequencing were conducted to explore the underlying mechanisms. Notably, CA markedly reduced serum uric acid (SUA), serum creatinine (SCr) and blood urea nitrogen (BUN) levels and alleviated renal and intestinal histopathological damage. In the kidney, CA upregulated ATP‑binding cassette sub‑family G member 2 (ABCG2), and downregulated glucose transporter 9 (GLUT9) and urate transporter 1 expression (URAT1). In the intestine, CA increased ABCG2, PDZ domain containing 1 (PDZK1) and tight junction protein expression, while decreasing GLUT9, suggesting improved urate excretion and barrier integrity. 16S ribosomal RNA sequencing revealed that CA was associated with increased gut microbial diversity and reduced abundance of potentially harmful bacteria, including . Phylogenetic Investigation of Communities by Reconstruction of Unobserved States‑based prediction suggested accompanying shifts in microbial functions related to transport and metabolism. In conclusion, these findings suggested that CA may exert beneficial effects on HUA involving regulation of renal and intestinal urate transport, improvement of intestinal barrier function and favorable modulation of gut microbiota. CA may therefore serve as a potential candidate for functional food development or therapeutic strategies against HUA. - Source: PubMed
Publication date: 2026/08/21
Yu XuezhiZhang YangSun KonchunYang RuiLi XingdeChen XiuzhenLi TiantianYang XiaoleiLi MingLiu LuLi FeiShen Baochun - Gastrointestinal (GI) cancers remain a leading cause of cancer-related mortality worldwide, with limited therapeutic options for advanced disease due to tumor heterogeneity, metastasis, cancer stemness, and acquired drug resistance. Cyclin-dependent kinases 7 and 9 (CDK7/9) are key regulators of transcription and cell-cycle progression, and their aberrant activation sustains oncogenic transcriptional programs. GNE-3511 is a dual CDK7/9 inhibitor with favorable pharmacokinetics, making it a promising therapeutic candidate for cancer treatment. The aim of the study is to investigate the anticancer efficacy and molecular mechanisms of GNE-3511 in gastrointestinal cancer models. Anticancer activity was evaluated in colorectal (HCT116), hepatocellular (HepG2), gastric (NCI-N87), and pancreatic (PanC1) cancer cells using cell viability, cell-cycle, apoptosis, migration, sphere formation, cancer stem cell, and doxorubicin accumulation assays. Expression of genes and proteins associated with apoptosis, epithelial-mesenchymal transition (EMT), stemness, multidrug resistance, and CDK7/9 signaling was analyzed by RT-qPCR and immunoblotting. Therapeutic efficacy was validated in an HCT116 xenograft model, with molecular analyses confirming the underlying anticancer mechanisms. GNE-3511 treatment reduced cell viability in all GI cancer cell lines, with the greatest potency in HepG2 followed by HCT116 cells. Further, GNE-3511 treatment induced G1 or G2/M cell-cycle arrest and promoted apoptosis by increasing BAX expression and suppressing BCL2, MCL1, and Survivin. GNE-3511 significantly reduced CD133⁺ and CD90⁺ cancer stem cell populations, inhibited migration, spheroid formation, and downregulated the stemness- and EMT-associated regulators Nanog, Snail, Twist, Vimentin, and Zeb1. Moreover, GNE-3511 enhanced intracellular accumulation of doxorubicin by repressing the multidrug resistance transporters ABCB1, ABCC9, and ABCG2. In HCT116 xenografts, GNE-3511 markedly suppressed tumor growth while reproducing the molecular effects observed in vitro. Furthermore, GNE-3511 did not cause treatment-related abnormalities, indicating favorable safety. Mechanistically, GNE-3511 inhibited CDK7/9 signaling, resulting in RB hypophosphorylation, suppression of POLR2A, and depletion of the oncogenic transcriptional regulators cMyc and MCL1. GNE-3511 exerts potent anticancer activity by disrupting CDK7/9-dependent transcriptional programs that regulate proliferation, apoptosis, stemness, EMT, and multidrug resistance. These findings identify GNE-3511 as a potential lead candidate for the treatment of colorectal cancers. - Source: PubMed
Publication date: 2026/08/21
Sharma NidhiPanneerselvam SuriyaBharate Sandip BAndugulapati Sai Balaji