NIT1 Catalyzes the hydrolysis of the amide bond in N-(4-oxoglutarate)-L-cysteinylglycine (deaminated glutathione), a metabolite repair reaction to dispose of the harmful deaminated glutathione. Plays a role in cell growth and apoptosis: loss of expression promotes cell growth, resistance to DNA damage stress and increased incidence to NMBA-induced tumors. Has tumor suppressor properties that enhances the apoptotic responsiveness in cancer cells; this effect is additive to the tumor suppressor activity of FHIT. It is also a negative regulator of primary T-cells. Belongs to the carbon-nitrogen hydrolase superfamily. NIT1/NIT2 family. Detected in heart, brain, placenta, liver, skeletal muscle, kidney and pancreas. 5 alternatively spliced human isoforms have been reported. Note: This description may include information from UniProtKB.
Protein type: EC 3.5.-.-; Hydrolase
Chromosomal Location of Human Ortholog: 1q23.3
Cellular Component:  mitochondrion
Molecular Function:  hydrolase activity, acting on carbon-nitrogen (but not peptide) bonds, in linear amides; nitrilase activity
Biological Process:  nitrogen compound metabolic process
Reference #:  Q86X76 (UniProtKB)
Alt. Names/Synonyms: Deaminated glutathione amidase; dGSH amidase; MGC57670; NIT1; nitrilase 1; Nitrilase homolog 1
Gene Symbols: NIT1
Molecular weight: 35,896 Da
Basal Isoelectric point: 7.91  Predict pI for various phosphorylation states
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Protein Structure Not Found.

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