G6PD (aa 305 _ 318)
- Known as:
- Glucose-6-phosphate dehydrogenase (aa 305 _ 318)
- Catalog number:
- Y213759
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- G6PD ( 305 _ 318)
Related genes to: G6PD (aa 305 _ 318)
- Gene:
- APOLD1 NIH gene
- Name:
- apolipoprotein L domain containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ25138, DKFZP434F0318
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-23
- Date modifiied:
- 2016-10-05
- Gene:
- ATP13A1 NIH gene
- Name:
- ATPase 13A1
- Previous symbol:
- ATP13A
- Synonyms:
- KIAA1825, FLJ31858, CGI-152
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-12
- Date modifiied:
- 2016-02-11
- Gene:
- BMT2 NIH gene
- Name:
- base methyltransferase of 25S rRNA 2 homolog
- Previous symbol:
- C7orf60
- Synonyms:
- DKFZp762M126, FLJ31818
- Chromosome:
- 7q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2008-06-19
- Date modifiied:
- 2016-04-22
- Gene:
- C3orf52 NIH gene
- Name:
- chromosome 3 open reading frame 52
- Previous symbol:
- -
- Synonyms:
- FLJ23186, TTMP
- Chromosome:
- 3q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-30
- Date modifiied:
- 2016-09-30
- Gene:
- C10orf120 NIH gene
- Name:
- chromosome 10 open reading frame 120
- Previous symbol:
- -
- Synonyms:
- bA318C4.1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2018-03-22
Related products to: G6PD (aa 305 _ 318)
Related articles to: G6PD (aa 305 _ 318)
- Hepatic ischemia reperfusion injury (IRI) is a frequent complication of liver surgery and is strongly associated with poorer recipient survival. Sorafenib, a multi-kinase inhibitor, has been implicated in hepatic metabolic and redox regulation, yet its role in hepatic IRI remains unclear. Our study finds that middle-dose sorafenib protects the liver from IRI by reducing hepatic necrosis, inflammation, and apoptosis. Mechanistically, transcriptomic and metabolomics analyses confirm that middle-dose sorafenib enhances pentose phosphate pathway-mediated antioxidant activity through the c-rapidly accelerated fibrosarcoma (c-Raf)/heat shock protein 90 (HSP90)/glucose-6-phosphate dehydrogenase (G6PD) axis. Co-immunoprecipitation, Western blot, and confocal immunofluorescence analyses demonstrate the direct binding interaction between HA-c-Raf and Myc-HSP90, as well as between Flag-G6PD and Myc-HSP90. Meanwhile, the overexpression of HSP90 disrupts the benefits of sorafenib on hepatic IRI, and inhibition of G6PD also rescues its protective effect. Notably, in human liver transplant recipients, elevated HSP90 levels correlated with poor graft function and survival, supporting its clinical relevance. Furthermore, a novel oral nanoparticle delivery system, targeting the liver tissue, enhances the therapeutic efficacy of sorafenib, restoring liver enzyme levels by up to 76%. Collectively, these findings identify middle-dose sorafenib, particularly when delivered via the novel oral nanoplatform, as an effective strategy to mitigate hepatic IRI. - Source: PubMed
Publication date: 2026/06/21
Gao FengqiangDong LibinTan YawenZhang ZhenXu ShengjunLou ZijianWu YichaoChen SiyuZhuang LiLian ZhengxingZheng ShusenQiu NashaWang KaiXu Xiao - Transfusion-dependent anemia (TDA) in children is often attributed to hemoglobinopathies; however, a spectrum of non-hemoglobinopathy disorders can also lead to transfusion dependence, complicating diagnosis and management. In this article, we share our experience with such non-hemoglobinopathy causes of TDA. A retrospective chart review was conducted over five years (2018-2023) at a tertiary pediatric hematology center. Among 93 children identified with TDA, 80 had hemoglobinopathies, while 13 had alternative diagnoses. These included immune-mediated hematological disorders, marrow failure syndromes, congenital RBC/platelet defects, and systemic illnesses. Descriptive statistics summarized clinical and demographic data. Of the 93 children with TDA, 13 had non-hemoglobinopathy causes: immune-mediated disorders (AIHA, Evans syndrome, PRCA, = 4), marrow failure syndromes (sideroblastic anemia, dyskeratosis congenita, = 3), inherited red cell/platelet defects (G6PD deficiency, Glanzmann thrombasthenia, = 3), and systemic illnesses (vasculitis, Langerhans cell histiocytosis, hypereosinophilic syndrome, = 3). The mean age was 4 years 5 months, with a male-to-female ratio of 1.16:1. Hepatosplenomegaly was observed in 8/13 cases. Non-hemoglobinopathy causes of TDA are heterogeneous, encompassing systemic, immune, genetic, and marrow failure disorders. Structured diagnostic evaluation is critical to distinguish them from hemoglobinopathies, enabling accurate treatment and improved outcomes. - Source: PubMed
Publication date: 2025/10/13
Misra AroonimaGoel NehaPrabhakar PrashantDandriyal RashmiRishi BhavikaSingh AmitabhBaruah RitamoniChopra NidhiMehndiratta SumitRay SanghamitraDas SammanayKriplani Kushal - High total dose primaquine (PQ 7 mg/kg) over 7 days can improve treatment adherence and reduce malaria recurrences. We evaluated the safety of pre-treatment glucose-6-phosphate dehydrogenase (G6PD) testing followed by high-dose primaquine for malaria in Indonesia and Papua New Guinea. - Source: PubMed
Publication date: 2026/06/11
Fransisca LionyOme-Kaius MariaLaman MosesPoespoprodjo Jeanne RiniPasaribu Ayodhia PSutanto IngeMalai MaryNelwan ErniAdella JacklynAbegini CynthiaAinur FramitaAmdara YolyneAngeline SherleyBrown KatelynBurdam Faustina HCurry EllaDaimen MartinDaly PaulDo ThyDori AnnieDouglas Nicholas MHuegel HeikeHutagalung Azkarunia PJambert ElodieJimanto VincentKaro ValiKenangalem EnnyKelebi TrevorKisomb JacobLaksono IdaLee GrantLey BenediktMannion KyliePlinduo JuliusPukai IrenePutri AdelaRajasekhar MeghaRonkentou SharolRosens EvelienSakalidis Vanessa SSatyagraha AriSimpson Julie ATheodora MinervaUbra ReynoldVakore NormanWansom TanyapornDuparc StephanRobinson Leanne JPrice Ric N - Glutathione (GSH) metabolism is closely associated with tumor behavior in hepatocellular carcinoma (HCC). HCC is the third fatality reason and the sixth incidence rank in global tumor ranking. Our study explored the connection between glutathione metabolism genes (GMGs) expression and HCC progression and prognosis. - Source: PubMed
Publication date: 2026/06/16
Li XiaolongTang JiayanQin HuotangHuang YuLi MinqingYang ZaiyongMeng JialiLi Ling - Metabolic reprogramming, especially the upretoning and functional reshaping of glycolysis, is the cornerstone of cancer progression, driving proliferation, invasion and metastasis. This review systematically analyzes the Warburg effect. This metabolic transformation promotes the progression of malignant tumors by enhancing glucose uptake, lactate production and microenvironmental remodeling. We elaborated on the molecular basis of this process, focusing on the oncogenic dysregulation of key glycolytic enzymes such as hexokinase 2 (HK2), phosphofructose kinase-1, pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA). These malfunctions are usually driven by hyperactive signaling pathways such as PI3K/AKT/mTOR and HIF-1α. This metabolic remodeling also actively shapes the tumor microenvironment (TME) by promoting acidosis, inhibiting anti-tumor immunity and stimulating angiogenesis. Intermediate metabolites in the process of glycolysis can also be used as signal nodes to regulate epithelial-mesenchymal transition (EMT) and maintain the plurity of cancer stem cells (CSC). The cyclic flux of the pentose phosphate pathway (PPP) and the truncated tricarboxylic acid (TCA) cycle flux further highlight the metabolic flexibility inherent in malignant cells. Finally, we critically evaluated emerging treatment strategies for these glycolysis vulnerabilities, including inhibitors of HK2, glucose-6-phosphate dehydrogenase (G6PD), fructose-2,6-diphosphatase3 (PFKFB3) and LDHA. This review reinforces the central position of glycolysis metabolism and emphasizes the potential of tumor treatment. - Source: PubMed
Publication date: 2026/06/19
Long YuxuanXu JianxiongXu ZenanSu ZhengdingLi WenfangLi Jinyao