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
- Hyperuricemia (HUA), a metabolic disorder associated with gout and cardiometabolic diseases, has become an important target for the development of food-derived functional ingredients. Pall, a widely consumed edible medicinal plant, has attracted attention as a potential source of urate-modulating compounds; however, its key active compounds and their urate-related activities remain unclear. In this study, through comprehensive phytochemical profiling, 20 compounds were isolated from and systematically evaluated using xanthine oxidase (XO) inhibition and HK-2 cellular models. Among them, 1,2,3,4,6--pentagalloylglucose (PGG, 20) exhibited potent XO inhibitory activity, with an IC value of 8.11 μM. Molecular docking and 100 ns molecular dynamics simulations further supported the stable binding of PGG to the catalytic pocket of XO, suggesting its role in inhibiting UA production at the enzymatic level. To investigate the urate transport-related activity of the isolates, a UA-induced injury model was established in HK-2 cells. Paeoniflorin (PF, 1) showed the strongest protective effect, improving cell viability by 13.47%. Western blot analysis showed that PF modulated the expression of urate transport-related proteins in HK-2 cells by decreasing the levels of the reabsorption-associated transporters URAT1 and GLUT9 and increasing the levels of the secretion-associated transporters OAT1 and ABCG2. In conclusion, these findings identify PGG and PF as two representative constituents of with distinct urate-related activity profiles in enzymatic and cellular models, respectively. This study provides a chemical and preliminary functional basis for the future development and quality evaluation of -derived functional ingredients targeting urate metabolism. - Source: PubMed
Publication date: 2026/08/11
Xu RuolingJin TingtingWang JingwenJi TingRen FucaiLi Ning - Current pharmacotherapies for hyperuricemia (HUA) are limited by variable efficacy and adverse effects, highlighting the urgent need for novel therapeutic targets and agents. The natural product saffron floral bio-residue (SFB) has demonstrated anti-hyperuricemic potential, but the underlying molecular mechanism remains unclear. - Source: PubMed
Publication date: 2026/08/04
Chen NaXiang JunjieLi JiaqiZhang LiLi YaliHao JinpingWei PengchengZhang LanGao Dan - Monocarboxylate transporters (MCTs) have been associated with cancer cell migration, invasion, and metastases with poor prognoses in various cancers. MCT1 and MCT4 have been identified as potential cancer markers and drug targets; several medicinal chemistry campaigns have provided drug candidates to pre-clinical and clinical stages. However, ligand development for MCTs is stalling, and several reasons can be identified, e.g., ultra-high potency-triggered on-target toxicity and compensation, isoform unselectivity, ubiquitous MCT expression, unspecificity over other targets, and MCTs-mediated multidrug resistance (MDR). The aim of the present study was the design of 2-azaindole (i.e., indazole) and 7-azaindole derivatives with moderate and balanced potency against MCT1 and MCT4, designed-out off-target effects on ATP-binding cassette (ABC) transporters, and efficacy in various in vitro cancer cell models. We identified cyanoacrylic acid ester-substituted indazoles that could optimally translate their functional MCT1 inhibition into efficacy against MCT1-expressing A-549 cancer cells. These compounds showed also efficacy against MCT4-expressing MDA-MB-231 cells, and correlation analyses on Hill slopes from functional and MDR reversal analyses pinpointed to a causal relationship between MCT1 and MCT4 inhibition and triggered cancer cell death. Glucose supplementation reversed cancer cell toxicity, while lead compounds could sensitize cancer cells toward doxorubicin and metformin. Strikingly, no inhibition of the ABC transporters ABCB1, ABCC1, and ABCG2 could be detected, and molecular docking analyses demonstrated interaction with the MCT1 drug binding pocket in a non-covalent manner. - Source: PubMed
Publication date: 2026/07/19
Latambale GaneshStefan KatjaGopakumar GopikaStefan Sven MarcelJuvale Kapil - Colon cancer (CC) remains a leading cause of cancer-related mortality worldwide, driven largely by the complex interactions within the tumor microenvironment (TME). Fibroblast activation protein (FAP) is highly expressed in cancer-associated fibroblasts (CAFs) and is associated with poor prognosis, yet its role in coordinating immune evasion and cancer stemness remains to be fully elucidated. - Source: PubMed
Publication date: 2026/08/06
Ding QianLu Qingyan - Cholangiocarcinoma (CCA) is a biliary cancer with a poor prognosis and marked chemoresistance. The transcription factor SOX17, which is essential for cholangiocyte differentiation, is frequently downregulated in CCA, as is the case with several tumor suppressor genes. This study provides a proof-of-concept for further development of cellular therapeutic strategies to restore SOX17 expression in CCA cells. For this aim, we used EGI-1 cells as the target cell model derived from extrahepatic CCA. Recombinant Tat-SOX17 protein was first produced in bacteria and purified using Ni-NTA affinity columns and asymmetric flow-field-flow fractionation. Tat-SOX17 entered EGI-1 cells and reached their nucleus. The addition of the α-fetoprotein signal peptide (AFPsp) to the chimeric protein enabled the efficient secretion of the fusion protein formed by AFPsp, SOX17, and reverse Tat (Tat) by donor cells. For the production of secretome enriched in AFPsp-SOX17-Tat protein, HEK293T cells, derived from embryonic kidney, were used. In EGI-1 cells cultured in the presence of this secretome, target gene expression, cell cycle progression, apoptosis, proliferation, colony formation, and cell migration were assessed. Protein expression and localization were analyzed by Western blotting and immunofluorescence. AFPsp-SOX17-Tat enters EGI-1 cells, reaches their nucleus, and modulates the expression of SOX17-dependent genes, such as ABCB1 and ABCG2. Moreover, a marked reduction in proliferation and colony-forming ability was found. In contrast, no significant effect on cell cycle progression, apoptosis, or cell migration was observed. Similar treatment of immortalized human cholangiocytes also increased their SOX17 content, resulting in upregulation of the cholangiolar marker cytokeratin 7 (CK7), but did not affect their proliferation rate. In conclusion, using chimeric proteins such as AFPsp-SOX17-Tat, which contain components for secretion from donor cells and entry into target cancer cells, can provide a promising approach for treating tumors such as CCA, which are characterized by reduced expression of tumor suppressor genes, including SOX17. - Source: PubMed
Publication date: 2026/08/04
Peleteiro-Vigil AnaOrtiz-Rivero SaraIzquierdo-Mateo YaniraSanchez-Vicente LauraGonzález-Sánchez EsterVaquero JavierArevalo Juan CarlosBriz OscarMonte Maria JMarin Jose J GHerraez Elisa