GSTM5 and GSTM3

Number of citations of the paper that reports this interaction (PMID 25416956)
0

Data Source:
BioGRID (two hybrid)

		GSTM5	GSTM3
Gene Name		glutathione S-transferase mu 5	glutathione S-transferase mu 3 (brain)
Image		No pdb structure
Gene Ontology Annotations	Cellular Component	Cytosol	Nucleus Cytoplasm Cytosol Sperm Fibrous Sheath Extracellular Vesicular Exosome
	Molecular Function	Glutathione Transferase Activity	Glutathione Transferase Activity Enzyme Binding Identical Protein Binding Protein Homodimerization Activity Glutathione Binding
	Biological Process	Glutathione Metabolic Process Xenobiotic Metabolic Process Small Molecule Metabolic Process Glutathione Derivative Biosynthetic Process	Glutathione Metabolic Process Xenobiotic Metabolic Process Establishment Of Blood-nerve Barrier Nitrobenzene Metabolic Process Xenobiotic Catabolic Process Response To Estrogen Small Molecule Metabolic Process Cellular Detoxification Of Nitrogen Compound Glutathione Derivative Biosynthetic Process
Pathways		Defective OPLAH causes 5-oxoprolinase deficiency (OPLAHD) Defective AHCY causes Hypermethioninemia with S-adenosylhomocysteine hydrolase deficiency (HMAHCHD) Defective TPMT causes Thiopurine S-methyltransferase deficiency (TPMT deficiency) Defective MAT1A causes Methionine adenosyltransferase deficiency (MATD) Defective UGT1A4 causes hyperbilirubinemia Glutathione conjugation Metabolic disorders of biological oxidation enzymes Phase II conjugation Defective UGT1A1 causes hyperbilirubinemia Defective SLC35D1 causes Schneckenbecken dysplasia (SCHBCKD) Biological oxidations Defective GCLC causes Hemolytic anemia due to gamma-glutamylcysteine synthetase deficiency (HAGGSD) Defective GGT1 causes Glutathionuria (GLUTH) Defective GSS causes Glutathione synthetase deficiency (GSS deficiency)	Defective OPLAH causes 5-oxoprolinase deficiency (OPLAHD) Defective AHCY causes Hypermethioninemia with S-adenosylhomocysteine hydrolase deficiency (HMAHCHD) Defective TPMT causes Thiopurine S-methyltransferase deficiency (TPMT deficiency) Defective MAT1A causes Methionine adenosyltransferase deficiency (MATD) Defective UGT1A4 causes hyperbilirubinemia Glutathione conjugation Metabolic disorders of biological oxidation enzymes Phase II conjugation Defective UGT1A1 causes hyperbilirubinemia Defective SLC35D1 causes Schneckenbecken dysplasia (SCHBCKD) Biological oxidations Defective GCLC causes Hemolytic anemia due to gamma-glutamylcysteine synthetase deficiency (HAGGSD) Defective GGT1 causes Glutathionuria (GLUTH) Defective GSS causes Glutathione synthetase deficiency (GSS deficiency)
Drugs			Glutathione
Diseases
GWAS
Protein-Protein Interactions		2 interactors: AMOTL2 GSTM3	6 interactors: GSTM1 GSTM2 GSTM4 GSTM5 SH3GL2 UCHL5
Entrez ID		2949	2947
HPRD ID		00711	00712
Ensembl ID		ENSG00000134201	ENSG00000134202
Uniprot IDs		P46439 Q5T8R2	P21266 Q6FGJ9
PDB IDs			3GTU
Enriched GO Terms of Interacting Partners?		Cellular Detoxification Of Nitrogen Compound Nitrobenzene Metabolic Process Detoxification Of Nitrogen Compound Establishment Of Blood-nerve Barrier Xenobiotic Catabolic Process Glutathione Derivative Biosynthetic Process Hippo Signaling Endothelial Cell Development Glutathione Metabolic Process Endothelial Cell Differentiation Endothelium Development Peripheral Nervous System Development Xenobiotic Metabolic Process Cellular Response To Xenobiotic Stimulus Response To Xenobiotic Stimulus Peptide Metabolic Process Response To Toxic Substance	Glutathione Derivative Biosynthetic Process Nitrobenzene Metabolic Process Glutathione Metabolic Process Xenobiotic Catabolic Process Xenobiotic Metabolic Process Cellular Response To Xenobiotic Stimulus Response To Xenobiotic Stimulus Peptide Metabolic Process Cellular Detoxification Of Nitrogen Compound Cellular Modified Amino Acid Metabolic Process Cellular Amide Metabolic Process Detoxification Of Nitrogen Compound Sulfur Compound Metabolic Process Catabolic Process Cellular Response To Stimulus Response To Toxic Substance Small Molecule Metabolic Process Regulation Of Skeletal Muscle Contraction By Regulation Of Release Of Sequestered Calcium Ion Response To Stimulus Biosynthetic Process Positive Regulation Of Ryanodine-sensitive Calcium-release Channel Activity Cellular Nitrogen Compound Metabolic Process Regulation Of Skeletal Muscle Contraction Negative Regulation Of Ryanodine-sensitive Calcium-release Channel Activity Cellular Response To Caffeine Nitrogen Compound Metabolic Process Relaxation Of Cardiac Muscle Negative Regulation Of Calcium Ion Transmembrane Transporter Activity Regulation Of Cardiac Muscle Contraction By Regulation Of The Release Of Sequestered Calcium Ion Cellular Response To Stress Negative Regulation Of Cation Channel Activity Forebrain Morphogenesis Relaxation Of Muscle Positive Regulation Of Calcium Ion Transmembrane Transporter Activity Regulation Of Cardiac Muscle Contraction By Calcium Ion Signaling Lateral Ventricle Development Regulation Of Release Of Sequestered Calcium Ion Into Cytosol By Sarcoplasmic Reticulum Response To Caffeine Regulation Of Ryanodine-sensitive Calcium-release Channel Activity Regulation Of Receptor Internalization Cellular Response To Organic Substance Cellular Response To Growth Factor Stimulus Positive Regulation Of Cation Channel Activity Response To Growth Factor Synaptic Vesicle Endocytosis Synaptic Vesicle Recycling Cellular Response To Alkaloid Negative Regulation Of Transporter Activity Negative Regulation Of Calcium Ion Transport Brain Morphogenesis
Tagcloud ?			5r acquire bax clonogenic exact facilitation fractionated hcc hepatoma immunoblotting irradiation lymphocytic modality p27 parental pivotal plc prf radiation radioresistance radioresistant radiosensitivity radiotherapy reversing rt sensitized sensitizing transferase
Tagcloud (Difference) ?			5r acquire bax clonogenic exact facilitation fractionated hcc hepatoma immunoblotting irradiation lymphocytic modality p27 parental pivotal plc prf radiation radioresistance radioresistant radiosensitivity radiotherapy reversing rt sensitized sensitizing transferase
Tagcloud (Intersection) ?