Monoclonal Mouse ABCG2 Antibody
- Known as:
- Monoclonal Mouse ABCG2 Antibody
- Catalog number:
- abx000055
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Monoclonal Mouse ABCG2 Antibody
Related genes to: Monoclonal Mouse ABCG2 Antibody
- 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: Monoclonal Mouse ABCG2 Antibody
Related articles to: Monoclonal Mouse ABCG2 Antibody
- seed cake is a major byproduct of the oil industry, often underutilized despite its richness in bioactive compounds. This study investigated the therapeutic effects and underlying mechanisms of seed cake extract (SCE) on potassium oxonate/hypoxanthine-induced hyperuricemia and renal injury in mice. SCE administration significantly reduced serum uric acid levels and improved renal function parameters (creatinine and blood urea nitrogen). Mechanistically, SCE inhibited hepatic xanthine oxidase and adenosine deaminase activities and modulated renal urate transporters by downregulating URAT1 and GLUT9 while upregulating OAT1 and ABCG2, thereby inhibiting uric acid synthesis and facilitating its excretion. UHPLC-MS/MS analysis identified 134 chemical constituents in SCE, primarily phenylpropanoids and polyketides. Integrated network pharmacology predicted the involvement of inflammatory pathways, which was validated in vivo. The results confirmed that SCE alleviated renal oxidative stress and inflammation by activating the Nrf2/Keap1 signaling pathway and suppressing the NLRP3 inflammasome. These findings demonstrate that SCE exerts potent anti-hyperuricemic and nephroprotective effects through multi-target regulation, supporting its potential as a functional food ingredient. - Source: PubMed
Publication date: 2026/05/18
Mai LitingXie YouliangZhang YingzhongNi ChenXu YingXu LieqiangLin GuoshuLin YinsiSu ZirenWang JingRen Mihong - Hyperuricemia is a metabolic disorder caused by the malfunction of uric acid metabolism. It is a common risk factor for gout and kidney disease. Currently, first-line pharmacotherapies for hyperuricemia, such as xanthine oxidase inhibitors (e.g., allopurinol and febuxostat) and uricosuric agents (e.g., benzbromarone), effectively lower serum uric acid levels. However, their clinical use is often limited by adverse effects, including hepatorenal toxicity, gastrointestinal disturbances, and hypersensitivity reactions. These limitations highlight the need for safer, better-tolerated therapeutic options. In this context, plant-derived interventions with multi-target mechanisms and favourable safety profiles have gained increasing research interest. Early studies suggest that the leaves of the traditional edible medicine, Xanthoceras sorbifolium Bunge (X. sorbifolium), may be promising for treating HUA. However, their clinical efficacy and mechanism of action remain to be clearly established. - Source: PubMed
Publication date: 2026/05/15
Liu YuquanHua ChunleiWu YiLv XinliangHei DongxuQiao LeiHan GuoqingA RuhanXie YingLi Minhui - Growing evidence has revealed that DEAD-box RNA helicase 5 (DDX5, also known as p68) and ubiquitin-conjugating enzyme E2T (UbE2T) are two emerging and highly promising cancer therapeutic targets. This article provides the first comprehensive review of the physical and functional relationship between these two cancer targets, further refining their therapeutic potentials in solid cancers. In addition, the consequences of simultaneously degrading DDX5 and UbE2T proteins by the small-molecule dual molecular glue degrader FL118 in difficult-to-treat advanced cancers are presented.Specifically, this article reviews: (1) the roles of DDX5 and UbE2T in diverse cancer DNA repair pathways; (2) the physical binding relationship and potential functional roles of DDX5 in topoisomerase regulation; (3) the involvement of DDX5 in EZH2- and NANOG-associated prostate cancer stem cell (PCSC)-driven neuroendocrine prostate cancer (NEPC), castration-resistant prostate cancer (CRPC), and metastatic CRPC (mCRPC); (4) the contributions of DDX5 and UbE2T to inflammatory and immune regulation within the tumor microenvironment (TME); (5) FL118 as a small-molecule dual molecular glue degrader selectively targeting both DDX5 and UbE2T; (6) the high efficacy of FL118 against multiple difficult-to-treat advanced and metastatic cancers, including advanced colorectal cancer (CRC), pancreatic ductal adenocarcinoma (PDAC), osteosarcoma, Ewing sarcoma, ovarian cancer, and glioma/glioblastoma; (7) the resistance of ABCG2-expressing cancer cells to common anticancer agents but not to FL118; (8) the favorable pharmacokinetic and toxicology profiles of FL118 in mice, rats, and dogs; (9) the distinct functions of DDX5 in normal tissues, cells, and organs versus cancer; and (10) FL118 as a drug platform enabling the development of novel analogs and derivatives.Based on this review, we conclude that DDX5 and UbE2T represent superior anticancer therapeutic targets, and that the high efficacy of FL118 against multiple difficult-to-treat cancers is attributable to its function as a bona fide small-molecule dual molecular glue degrader that physically targets and degrades both DDX5 and UbE2T. Strikingly, this activity is observed regardless of the expression status of ABC transporter proteins, ABCG2/BCRP, ABCB1/Pgp/MDR1, and/or ABCC1/MRP1 in cancer cells. - Source: PubMed
Publication date: 2026/05/18
Li FengzhiLing XiangChakraborty SayanTang Dean GMcLean KarenWu WenjieSule NorbertVadehra DeepakFountzilas ChristosGupta AjayTwist ClareOhm JoyceChatta GurkamalAbrams Scott I - Regulatory T cells (Tregs) are key mediators of immune suppression in cancer and are frequently elevated in hematologic malignancies, including acute and chronic leukemias, however, their role in modulating the leukemic cell phenotype and therapy response remains unclear. This study investigated whether natural Tregs (nTregs), in vitro-generated CD4CD25Foxp3 Tregs (iTregs), and type 1 regulatory T (Tr1) cells directly modulate the phenotype, viability and drug response of the K562 chronic myeloid leukemia cell line in vitro. K562 cells were cultured either in direct co-culture with Treg subsets or in their culture supernatants, followed by flow cytometric assessment of stemness-associated and progression/drug-resistance-related markers. Anti-TGF-β1 or anti-IL-10 blocking antibodies were used to assess cytokine-dependent mechanisms. Functional effects were evaluated using an MTT-based assay under drug-free conditions or after treatment with daunorubicin or gemcitabine. Natural Tregs increased the proportion of CD34, PDGFRβ, ABCG2 and VEGFR1⁺ K562 cells. Neutralization of TGF-β1 in the co-culture system partially attenuated the nTreg-associated upregulation of PDGFRβ and ABCG2. iTregs increased ABCG2 expression, which was also reduced upon TGF-β1 blockade. Tr1 cells increased the proportion of CD24⁺ cells, upregulated PDGFRβ and ABCG2, and increased K562 cell metabolic activity/viability under drug-free conditions. All Treg subsets attenuated daunorubicin cytotoxicity, whereas reduced sensitivity to gemcitabine was observed only in iTreg- and Tr1-containing cultures. These findings suggest that Treg cell subsets may directly promote stemness-associated and drug-tolerance-related features in K562 cells in vitro, supporting a tumor-promoting role within the leukemia microenvironment and warranting further validation in primary leukemia samples and in vivo models. - Source: PubMed
Publication date: 2026/05/12
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Publication date: 2026/05/14
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