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NIT1 encodes a member of the nitrilase protein family with homology to bacterial and plant nitrilases, enzymes that cleave nitriles and organic amides to the corresponding carboxylic acids plus ammonia.
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NIT1/NIT2 (show NIT2 Proteins) heteromers catalyse the hydrolysis of indole-3-acetonitrile and beta-cyanoalanine.
Data show that cisplatin response was enhanced in human lung cancer cells when Nit1 was knocked down and mice Nit1-/-:KrasG12D/+ tumors showed increased sensitivity to cisplatin in vivo.
Human NIT1/2 are not involved in the metabolism of vildagliptin.
Nit1 and Fhit share tumor suppressor signaling pathways, while localization of the NIT1 gene at a stable chromosome site explains the paucity of gene alterations and in frequent loss of expression of the NIT1 gene in human malignancies.
genetic deficiency results in T cell hyperproliferative responses induced by TCR stimulation, spontaneous cell cycle entry and enhanced cell cycle progression
the extent of tumor susceptibility due to Nit1 and Fhit deficiency is additive
NIT1 regulates the exit from proliferation, genome stability and plant development.
This gene encodes a member of the nitrilase protein family with homology to bacterial and plant nitrilases, enzymes that cleave nitriles and organic amides to the corresponding carboxylic acids plus ammonia. Multiple transcript variants encoding different isoforms have been found for this gene.
, Nit protein 1
, nitrilase homolog 1
, hypothetical protein
, nitrilase 1Nitrilase 4
, nitrilase homolog 1-like