Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Regulation of gamma-glutamylcysteine synthetase regulatory subunit (GLCLR) gene expression: identification of the major transcriptional start site in HT29 cells.
Overexpression of gamma-glutamylcysteine synthetase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-kappa B and activator protein-1.
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GCS overexpression blocks TNF-induced NF-kappa B activation
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GCS overexpression suppresses TNF-induced apoptosis and caspase-3 activation
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Cellular redox status controlled by glutathione affects pleiotropic TNF actions
Oxidant stress induces gamma-glutamylcysteine synthetase and glutathione synthesis in human bronchial epithelial NCI-H292 cells.
Association of polymorphism in glutamate-cysteine ligase catalytic subunit gene with coronary vasomotor dysfunction and myocardial infarction.
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GCLC -129T polymorphism has lower promoter activity in response to oxidants
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Associated with impaired endothelium-dependent coronary vasodilation
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Risk factor for myocardial infarction
A novel missense mutation in the gamma-glutamylcysteine synthetase catalytic subunit gene causes both decreased enzymatic activity and glutathione production.
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R127C mutation causes decreased enzymatic activity and GSH production
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Mutation lies within a cleft near the binding site
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Causes hemolytic anemia (CNSHA7)
Knockdown of glutamate-cysteine ligase by small hairpin RNA reveals that both catalytic and modulatory subunits are essential for the survival of primary neurons.
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shRNA knockdown of GCLC or GCLM causes neuronal apoptosis
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Both subunits essential for neuronal survival
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Rescue by gamma-glutamylcysteine or GSH ethyl ester
Gamma-glutamylcysteine synthetase deficiency and hemolytic anemia.
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GCLC deficiency causes hemolytic anemia
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Decreased GSH in lymphoblasts and fibroblasts
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Clinical expression may be pleomorphic
Inactivation of human gamma-glutamylcysteine synthetase by cystamine. Demonstration and quantification of enzyme-ligand complexes.
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Detection of enzyme-Mg2+ complexes
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Detection of enzyme-ATP-glutamate complexes
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Magnesium ion confers protection against cystamine inactivation
Architecture of the human interactome defines protein communities and disease networks.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
gamma-Glutamylcysteine synthetase and active transport of glutathione S-conjugate are responsive to heat shock in K562 erythroid cells.
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Heat shock increases gamma-GCS activity 1.7-fold
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Erythropoietin decreases gamma-GCS activity to 64% of control
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mRNA induction correlates with enzymatic activity changes
Expression and purification of human gamma-glutamylcysteine synthetase.
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Co-expression and purification of human GCLC-GCLM holoenzyme
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Km values determined - glutamate 1.8 mM, cysteine 0.1 mM, ATP 0.4 mM
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Specific activity greater than 1500 units/mg
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Feedback inhibited by glutathione
Identification of an important cysteine residue in human glutamate-cysteine ligase catalytic subunit by site-directed mutagenesis.
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Cys553 important for GCLC-GCLM heterodimer formation
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C553G mutation reduces holoenzyme activity
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Eight conserved cysteine residues analyzed
GCL ligates L-Glu to L-Cys
Defective GCLC does not ligate L-Glu to L-Cys
AcK-NFE2L2-dependent GCLC gene expression
Deep research report on GCLC