Ask about this productRelated genes to: G6PD protein
- Gene:
- G6PD NIH gene
- Name:
- glucose-6-phosphate dehydrogenase
- Previous symbol:
- -
- Synonyms:
- G6PD1
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: G6PD protein
Related articles to: G6PD protein
- Post cardiac arrest brain injury (PCABI) results from global ischemia-reperfusion. Circular RNAs (circRNAs) are stable regulators of post transcriptional networks that may modulate neuronal survival and metabolism after ischemic injury. We investigated the role and mechanism of mmu_circ_0000376 (circ_0000376) in PCABI. - Source: PubMed
Publication date: 2026/05/26
Lin LongZhao YingtongLiu XiongHuang XiaodongHuang XianweiPan MandongLin Jiyan - Pancreatic cancer remains one of the deadliest malignancies, with gemcitabine-based chemotherapy as a mainstay treatment for most patients, yet resistance emerges almost universally. A defining feature of pancreatic cancer is its dense, fibroblast-rich stroma, where heterogeneous cancer-associated fibroblasts (CAFs) actively shape tumor biology and therapeutic response. Here, we elucidated a stromal-metabolic mechanism through which chemoresistant CAFs confer gemcitabine resistance. A subset of mitophagy-competent CAFs enhanced pancreatic cancer gemcitabine resistance. The EMT transcription factor ZEB1 acted as a master regulator of the CAF-driven chemoresistance program, and it was upregulated and epigenetically activated through SETD1A-mediated H3K4 methylation in gemcitabine-resistant CAFs. ZEB1 promoted BNIP3-mediated mitophagy in CAFs, leading to increased secretion of nucleotides that competitively inhibited gemcitabine incorporation into cancer cells while simultaneously supplying pyrimidine metabolism substrates for pyrimidine metabolism. Concurrently, ZEB1 transcriptionally activated CXCL8, engaging the CXCR1/2-MEK/ERK pathway in tumor cells and further augmenting pyrimidine metabolism via the RRM1/E2F1/G6PD axis, collectively diminishing gemcitabine cytotoxicity. Notably, combined inhibition of CXCR1/2 or G6PD with gemcitabine robustly suppressed tumor growth and restored chemosensitivity both in vitro and in vivo. Together, these findings uncover a key stromal-metabolic axis in pancreatic cancer, linking CAF mitophagy activity to metabolic remodeling in tumor cells and identifying ZEB1 and its downstream network as actionable targets to overcome chemoresistance. - Source: PubMed
Publication date: 2026/05/27
Zhang ShaoboYuan HaoGuo MuziZhou ZhijunHu YumengLv GaoyuanQi HaoranGuo YuanyuanHan JingBronze Michael SHouchen Courtney WLi MinLiu Mingyang - Sickle cell disease (SCD) is an inherited blood disorder characterized by the presence of sickle-shaped erythrocytes, leading to haemolytic anemia, vaso-occlusive crises, and multi-organ complications. In this study, we describe the lived experiences of persons with SCD (PwSCD) and their caregivers within their social and cultural contexts, aiming to uncover the factors that limit effective healthcare for tribal communities in India. - Source: PubMed
Publication date: 2026/05/27
Swathi VAggarwal PoojaKhanum FahimaBhat Deepa - Microbial communities and tailings multifunctionality are prerequisites for iron tailings' eco-engineering into technosols, but how organic matter supplementation improves these remains unclear. This study explored multifunctional enhancement, microbial enrichment, and driving mechanisms via microcosm experiments with fulvic acid (FL), rice husk (RC), and FL + RC (FLRC). Over 60-day incubation, tailings' multifunctional index showed exponential growth in FL treatment and pseudo-first-order kinetics in RC/FLRC, attributed to the stronger organic matter decomposition potential in FL (3 × 10) than RC (1.4 × 10) and FLRC (0). Network analysis revealed rare microorganisms (relative abundance < 1%, bacterial genera of Sericytochromatia and Parasegetibacter, fungal genera of Fusarium and Cystobasidium) had the strongest correlations with physicochemical factors (r = 0.97), indicating the rare microorganisms instead of dominant taxa drive tailings multifunctionality. Mantel tests revealed external carbon sources regulate the tailings carbon cycle via pgk, cellulase, and pdh genes, while the microenvironment directly propels it through cs, g6pd, ms and cat genes. Collectively, these findings clarify the key drivers regulating ecological functions of iron tailings, providing a sustainable strategy for tailings ecological restoration and resource utilization. - Source: PubMed
Publication date: 2026/05/25
Liu HengZhang XiaoshanLiu MingbaoLi FengYe YuanyuanMa ZimengQiao Chengfang - Since NO can modulate mesenchymal cell function, we posit that NO can modulate gene expression associated with excitation-contraction coupling. Our study shows that treating asthma-derived HASMCs with a low dose of NO plus sGC stimulator BAY-41, in most cases sensitized smooth muscle sGC towards activation via an elevated sGC heterodimer and in some cases also improved sGCβ1, catalase, Cyb5r3 or Trx1 expression (n=24 non-asthma and n=25 asthma). Interestingly we found that majority of asthma HASMCs showed a marked downregulation of G6PD expression inducing a low GSH/GSSG ratio in asthma, and these findings were replicated in murine lungs of allergic asthma (OVA and CFA/HDM). Studies with HEK/COS-7 cells showed G6PD synergizing with hsp90 in enabling sGC heme-maturation. G6PD overexpression in HASMCs enhanced the sGC heterodimerization while silencing of endogenous G6PD abrogated it. Complementation of these cellular results with whole animal models of G6PD deficiency or overexpression provided verification to our findings. Mouse lung tissue from the humanized variant of G6PD deficiency, V68M (G6PD A-deficiency) showed significant downregulation in the sGC heterodimer, with a concomitant reduction in its NO heme-dependent activity, thereby showing that G6PD deficiency lowers sGC heme. Conversely, G6PD overexpressing mouse lung tissue displayed an elevated sGC heterodimer and also showed a robust G6PD-sGCβ1 interaction, suggesting G6PD to be involved in the heme-maturation of sGCβ1. While G6PD maintains the cell redox by generating NADPH, its new role in regulating sGC maturation links sGC dysfunction in asthma to G6PD deficiency and may potentially uncover new targets for asthma treatment. - Source: PubMed
Publication date: 2026/05/11
Ghosh ArnabSumi Mamta PKoziol-White CynthiaTupta BlairWang LingGhosh ChaitaliJester William FPanettieri Reynold AStuehr Dennis J