Gene Ontology annotation through association of InterPro records with GO terms

Annotation inferences using phylogenetic trees

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt

Gene Ontology annotation based on curation of immunofluorescence data

Gene Ontology annotation based on curation of intracellular localizations of expressed fusion proteins in living cells

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Combined Automated Annotation using Multiple IEA Methods

UniProt text export for G6PD (P11413)

Cell growth and cholesterol metabolism in human glucose-6-phosphate dehydrogenase deficient lymphomononuclear cells.

Structural studies of glucose-6-phosphate and NADP+ binding to human glucose-6-phosphate dehydrogenase.

Production of inflammatory molecules in peripheral blood mononuclear cells from severely glucose-6-phosphate dehydrogenase-deficient subjects.

Mutation in G6PD gene leads to loss of cellular control of protein glutathionylation: mechanism and implication.

Large-scale proteomics and phosphoproteomics of urinary exosomes.

Defining the membrane proteome of NK cells.

ATM activates the pentose phosphate pathway promoting anti-oxidant defence and DNA repair.

Quantitative proteomic analysis of human substantia nigra in Alzheimer's disease, Huntington's disease and Multiple sclerosis.

Sex steroid hormone modulation of NADPH pathways in MCF-7 cells.

In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.

Ribose metabolism and nucleic acid synthesis in normal and glucose-6-phosphate dehydrogenase-deficient human erythrocytes infected with Plasmodium falciparum.

Regulation of G6PD acetylation by SIRT2 and KAT9 modulates NADPH homeostasis and cell survival during oxidative stress.

A proteome-scale map of the human interactome network.

Severe G6PD Deficiency Due to a New Missense Mutation in an Infant of Northern European Descent.

Aldolase B suppresses hepatocellular carcinogenesis by inhibiting G6PD and pentose phosphate pathways.

Substitution of arginine 219 by glycine compromises stability, dimerization, and catalytic activity in a G6PD mutant.

Biochemical variants of glucose-6-phosphate dehydrogenase giving rise to congenital nonspherocytic hemolytic disease.

Glucose 6-phosphate dehydrogenase activity in membranes of erythrocytes from normal individuals and subjects with Mediterranean G6PD deficiency.

G6PD multimers dehydrogenate G6P

AcK-NFE2L2-dependent P6GD gene expression

Dual NADPH oxidases DUOX1 and DUOX2 synthesize NAADP and are necessary for Ca(2+) signaling during T cell activation.

Glucose-6-phosphate dehydrogenase activity and NADPH/NADP+ ratio in liver and pancreas are dependent on the severity of hyperglycemia in rat.

Effect of anabolic steroid nandrolone decanoate on the properties of certain enzymes in the heart, liver, and muscle of rats, and their effect on rats' cardiac electrophysiology.

The pentose phosphate pathway in the endoplasmic reticulum.

Significance of the 5-phosphoribosyl-1-pyrophosphate pool for cardiac purine and pyrimidine nucleotide synthesis: studies with ribose, adenine, inosine, and orotic acid in rats.

Expression of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in oxidative stress induced by long-term iron toxicity in rat liver.

Involvement of mitochondrial permeability transition, glutathione status, pentose phosphate pathway and oxidative damage in the protective effect of fasting on the ischaemic-reperfused rat heart.

Peroxynitrite protects neurons against nitric oxide-mediated apoptosis. A key role for glucose-6-phosphate dehydrogenase activity in neuroprotection.

[Tissue-specific features of the pentose phosphate pathway in rats under acute alcoholic intoxication conditions].

Cardiac-specific hexokinase 2 overexpression attenuates hypertrophy by increasing pentose phosphate pathway flux.

Glucose-6-phosphate dehydrogenase and NADPH redox regulates cardiac myocyte L-type calcium channel activity and myocardial contractile function.