Affinage

NIT1

Deaminated glutathione amidase · UniProt Q86X76

Length
327 aa
Mass
35.9 kDa
Annotated
2026-04-29
78 papers in source corpus 10 papers cited in narrative 10 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NIT1 is a cytoplasmic and mitochondrial amidase that functions as a metabolite repair enzyme by specifically hydrolyzing deaminated glutathione (dGSH), a toxic byproduct generated by promiscuous side-reactions of various aminotransferases; NIT1-knockout cells and mice accumulate dGSH, confirming its non-redundant role in metabolite damage control (PMID:28373563, PMID:30692244). NIT1 also acts as a tumor suppressor: its deficiency accelerates cell proliferation, impairs caspase-dependent apoptosis and the Chk2 DNA damage checkpoint, and increases susceptibility to carcinogen-induced tumors in mice, with additive tumor suppression alongside FHIT (PMID:16864578, PMID:19479888). NIT1 suppresses colorectal cancer cell proliferation by recruiting SMAD2/3 to the TGFβ receptor via interaction with SARA, activating TGFβ1–SMAD2/3 signaling, and negatively regulates T cell proliferation and survival (PMID:29449642, PMID:19395373). Bi-allelic loss-of-function variants in human NIT1 cause a cerebral small vessel disease, linking its dGSH repair activity to neurological integrity (PMID:38430071).

Mechanistic history

Synthesis pass · year-by-year structured walk · 6 steps
  1. 2006 High

    Before this work, NIT1 was an uncharacterized nitrilase-family member with no known biological function; this study established that NIT1 acts as a tumor suppressor whose loss accelerates proliferation, elevates cyclin D1, blocks caspase-dependent apoptosis, and increases carcinogen-induced tumor incidence in mice.

    Evidence Nit1-knockout mouse kidney cells, carcinogen-induced tumor model, adenoviral rescue, caspase activity assays

    PMID:16864578

    Open questions at the time
    • Enzymatic substrate of NIT1 was unknown
    • Mechanism connecting NIT1 catalytic activity to apoptosis not defined
    • Whether NIT1 tumor suppression is independent of FHIT was unclear
  2. 2009 High

    Two studies clarified that NIT1 and FHIT suppress tumors through additive, distinct pathways—NIT1 loss specifically impairs the Chk2 DNA damage checkpoint—and that NIT1 negatively regulates T cell proliferation and apoptosis, broadening its role beyond epithelial tumor suppression.

    Evidence Fhit/Nit1 double-KO mouse tumor model, subcellular fractionation showing cytoplasmic/mitochondrial localization, Nit1-KO primary T cell functional assays

    PMID:19395373 PMID:19479888

    Open questions at the time
    • Enzymatic activity and substrate still unidentified
    • Whether checkpoint and apoptosis defects are direct or secondary remained unknown
    • T cell phenotype from single lab, not independently replicated
  3. 2017 High

    The central mechanistic question—what NIT1 catalyzes—was resolved: NIT1 is an amidase that specifically hydrolyzes deaminated glutathione (dGSH), a metabolite damage product of aminotransferase side-reactions, establishing NIT1 as a metabolite repair enzyme.

    Evidence In vitro enzymatic assay with recombinant NIT1, NIT1-KO cell lines (human and yeast), NIT1-KO mouse urine metabolomics

    PMID:28373563

    Open questions at the time
    • Whether dGSH accumulation explains the tumor suppressor and immune phenotypes was not tested
    • Structural basis for dGSH specificity not determined
    • Physiological consequences of dGSH accumulation in specific tissues unknown
  4. 2018 Medium

    A distinct signaling mechanism was proposed: NIT1 suppresses colorectal cancer proliferation by physically interacting with SARA and SMAD2/3 to activate TGFβ1 signaling, with a positive feedback loop in which SMAD3 binds the NIT1 promoter.

    Evidence Co-immunoprecipitation (NIT1–SARA, NIT1–SMAD2/3), ChIP of SMAD3 at NIT1 promoter, knockdown/overexpression in colorectal cancer cells and xenografts

    PMID:29449642

    Open questions at the time
    • Relationship between NIT1 enzymatic (amidase) activity and TGFβ signaling function not clarified
    • Single-lab Co-IP without reciprocal pulldown validation for SARA interaction
    • Whether TGFβ mechanism operates in normal tissues versus cancer context unknown
  5. 2023 Medium

    The long-suspected direct NIT1–FHIT physical interaction was confirmed with purified recombinant proteins, and NIT1 was shown to form a homotetramer, defining its quaternary structure.

    Evidence Purified recombinant protein co-purification, size exclusion chromatography, co-immunoprecipitation identifying shared partners Hsp60 and Ubc9

    PMID:36766695

    Open questions at the time
    • Functional significance of NIT1–FHIT complex and NIT1 tetramerization not established
    • Whether Hsp60 and Ubc9 interactions are functionally relevant or chaperone/quality-control artifacts is unclear
    • High-resolution structural data for the NIT1 tetramer or NIT1–FHIT complex lacking
  6. 2024 Medium

    The physiological importance of NIT1's metabolite repair function was demonstrated in humans: bi-allelic NIT1 loss-of-function causes cerebral small vessel disease with electron-dense vascular deposits, linking dGSH accumulation to neurological pathology.

    Evidence Exome sequencing of affected individuals, Western blot confirming absent NIT1 protein, urine metabolomics confirming dGSH accumulation, brain autopsy with electron microscopy

    PMID:38430071

    Open questions at the time
    • Causal mechanism connecting dGSH accumulation to vascular wall deposits not defined
    • Small number of families; broader phenotypic spectrum unknown
    • No rescue experiment in patient-derived cells

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown whether NIT1's tumor suppressor, immune-regulatory, and TGFβ signaling functions are mechanistically linked to its dGSH hydrolase activity or represent independent functions, and the structural basis for dGSH recognition is unresolved.
  • No separation-of-function mutant distinguishing catalytic from signaling roles
  • No crystal structure of NIT1 with substrate
  • Tissue-specific consequences of dGSH accumulation in brain versus immune versus epithelial compartments unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016787 hydrolase activity 2
Localization
GO:0005829 cytosol 3 GO:0005739 mitochondrion 1
Pathway
R-HSA-1430728 Metabolism 2 R-HSA-5357801 Programmed Cell Death 2 GO:0016787 hydrolase activity 1 R-HSA-162582 Signal Transduction 1
Partners
FHITHSP60SARASMAD2SMAD3UBC9

Evidence

Reading pass · 10 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2017 Mammalian Nit1 is an amidase that specifically hydrolyzes deaminated glutathione (dGSH), a metabolite damage product generated by the side-reaction of various aminotransferases. Nit1-KO cells (human and yeast) accumulate dGSH, and Nit1-KO mice excrete large amounts of dGSH in urine, establishing Nit1 as a metabolite repair enzyme. In vitro enzymatic assay with recombinant protein, Nit1-KO cell lines (human and yeast), Nit1-KO mouse urine metabolomics, identification of transaminases as dGSH-forming enzymes Proceedings of the National Academy of Sciences of the United States of America High 28373563
2019 Arabidopsis Nit1 (At4g08790) is an amidase with high and specific activity toward dGSH. Ablation of the Arabidopsis Nit1 gene causes massive accumulation of dGSH. Nit1 is dual-targeted to cytoplasm and plastids via alternative translation start sites, demonstrated by in vitro transcription/translation and confocal microscopy of Nit1-GFP fusions. Recombinant enzyme assay, Arabidopsis Nit1 knockout metabolomics, in vitro transcription/translation, confocal microscopy of GFP fusions The Biochemical journal High 30692244
2006 Mammalian Nit1 functions as a tumor suppressor. Nit1-deficient mouse kidney cells show accelerated proliferation, resistance to DNA damage stress, and increased cyclin D1 expression. Nit1 overexpression induces caspase-dependent apoptosis in vitro. Nit1 allele deficiency increases incidence of carcinogen-induced forestomach tumors in mice. Adenoviral re-expression of NIT1 induces apoptosis in Nit1-deficient cells, and FHIT re-expression induces apoptosis in Nit1-deficient cells (and vice versa), indicating Nit1-Fhit interaction is not essential for individual function. Nit1-knockout mouse cells, carcinogen tumor induction model, adenoviral overexpression, caspase activity assay, Western blot (cyclin D1) The Journal of biological chemistry High 16864578
2009 Nit1 and Fhit tumor suppressor activities are additive and affect distinct signaling pathways. Double-knockout (Fhit−/−Nit1−/−) mice develop more spontaneous and carcinogen-induced tumors than Fhit−/− mice alone. Nit1 is present in cytoplasm and mitochondria but not nuclei. Nit1-deficient cells fail to activate the pChk2 DNA damage checkpoint pathway upon hydroxyurea treatment. Double-knockout mouse tumor susceptibility assay, subcellular fractionation, Western blot (pChk2), carcinogen challenge Journal of cellular biochemistry High 19479888
2009 Nit1 acts as a negative regulator in primary T cells. Nit1-deficient T cells show compromised apoptosis induced by Fas or Ca2+ signals, spontaneous cell cycle entry, enhanced cell cycle progression, and hyperproliferative TCR-stimulated responses with elevated T cell activation markers. Nit1-knockout mouse T cells, apoptosis assays (Fas, Ca2+ stimuli), cell cycle analysis, flow cytometry for activation markers International immunology Medium 19395373
2018 NIT1 suppresses colorectal cancer cell proliferation by activating the TGFβ1-Smad2/3 signalling pathway. NIT1 recruits Smad2/3 to the TGFβ receptor by interacting with SARA and SMAD2/3. A positive feedback loop exists whereby SMAD3 directly binds to the NIT1 promoter and enhances NIT1 transcription. Co-immunoprecipitation (NIT1 with SARA and SMAD2/3), promoter ChIP assay, loss-of-function/gain-of-function in vitro and in vivo (xenograft), cell cycle and apoptosis assays Cell death & disease Medium 29449642
2023 Nit1 and Fhit physically interact directly, as demonstrated by biochemical co-purification. Purified recombinant human Nit1 forms a tetrameric structure by size exclusion chromatography. Nit1 and Fhit share common interaction partners Hsp60 and Ubc9, identified by co-immunoprecipitation. Purified recombinant protein interaction assay, size exclusion chromatography, co-immunoprecipitation Cells Medium 36766695
2024 Bi-allelic loss-of-function variants in human NIT1 cause a cerebral small vessel disease. Patient fibroblasts show absence of NIT1 protein by Western blot. Urine metabolic analysis confirms loss of NIT1 enzymatic function (dGSH repair). Brain autopsy revealed large electron-dense deposits in vessel walls of small and medium cerebral arteries. Exome sequencing, Western blot on patient fibroblasts, urine metabolomics, brain autopsy with electron microscopy Genetics in medicine : official journal of the American College of Medical Genetics Medium 38430071
2025 Nit1 functions as a metabolite repair enzyme hydrolyzing dGSH, a byproduct of transaminase side-reactions. The physiological significance is underscored by discovery that NIT1 deficiency in humans causes a neurological disorder (cerebral small vessel disease). Review/perspective citing prior biochemical reconstitution and human genetic studies Analytical biochemistry Medium 41390003
2025 Nit1 is localized to the cytoplasm in lung cancer cell lines (HBE, A549, H1299, H460, PC9) by immunofluorescent staining. Overexpression of Nit1 in H1299 cells promotes proliferation and invasion, upregulates MMP3, Slug, Snail, cyclin D1, cyclin D3, cyclin E, and downregulates E-cadherin, indicating regulation of EMT and cell cycle molecules. Immunofluorescence for subcellular localization, overexpression with Western blot for EMT and cyclin markers, proliferation and invasion assays Journal of Cancer Low 40740246

Source papers

Stage 0 corpus · 78 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1991 NIT-1, a pancreatic beta-cell line established from a transgenic NOD/Lt mouse. Diabetes 243 1647994
1997 Arabidopsis mutants resistant to the auxin effects of indole-3-acetonitrile are defective in the nitrilase encoded by the NIT1 gene. The Plant cell 127 9368415
2001 Enzymatic characterization of the recombinant Arabidopsis thaliana nitrilase subfamily encoded by the NIT2/NIT1/NIT3-gene cluster. Planta 115 11525507
1999 Tumor necrosis factor-alpha-activated cell death pathways in NIT-1 insulinoma cells and primary pancreatic beta cells. Endocrinology 99 10385418
1997 Expression of the arylsulphatase reporter gene under the control of the nit1 promoter in Chlamydomonas reinhardtii. Current genetics 70 9065390
2015 Graphene oxide inhibits hIAPP amyloid fibrillation and toxicity in insulin-producing NIT-1 cells. Physical chemistry chemical physics : PCCP 62 26625841
1984 Quantitative transfer of the molybdenum cofactor from xanthine oxidase and from sulphite oxidase to the deficient enzyme of the nit-1 mutant of Neurospora crassa to yield active nitrate reductase. The Biochemical journal 56 6234882
2009 Characterization of vesicles secreted from insulinoma NIT-1 cells. Journal of proteome research 47 19351151
2007 The role of G protein-coupled receptor 40 in lipoapoptosis in mouse beta-cell line NIT-1. Journal of molecular endocrinology 47 17556534
1992 Expression of chimeric genes by the light-regulated cabII-1 promoter in Chlamydomonas reinhardtii: a cabII-1/nit1 gene functions as a dominant selectable marker in a nit1- nit2- strain. Molecular and cellular biology 46 1406696
2015 STAT1-mediated down-regulation of Bcl-2 expression is involved in IFN-γ/TNF-α-induced apoptosis in NIT-1 cells. PloS one 45 25811609
2017 Nit1 is a metabolite repair enzyme that hydrolyzes deaminated glutathione. Proceedings of the National Academy of Sciences of the United States of America 42 28373563
2013 Wnt3a regulates proliferation, apoptosis and function of pancreatic NIT-1 beta cells via activation of IRS2/PI3K signaling. Journal of cellular biochemistry 41 23296977
2005 Imaging plant cell death: GFP-Nit1 aggregation marks an early step of wound and herbicide induced cell death. BMC plant biology 41 15796778
2006 Biological functions of mammalian Nit1, the counterpart of the invertebrate NitFhit Rosetta stone protein, a possible tumor suppressor. The Journal of biological chemistry 40 16864578
1997 Mechanisms of arginine-induced increase in cytosolic calcium concentration in the beta-cell line NIT-1. Diabetologia 37 9112013
2010 Over-expression of miR375 reduces glucose-induced insulin secretion in Nit-1 cells. Molecular biology reports 36 20221699
2016 The Influence of Stabilized Deconjugated Ursodeoxycholic Acid on Polymer-Hydrogel System of Transplantable NIT-1 Cells. Pharmaceutical research 33 26818840
2002 Functional IL-18 Is produced by primary pancreatic mouse islets and NIT-1 beta cells and participates in the progression towards destructive insulitis. Hormone research 33 12006705
2014 Jinlida granule inhibits palmitic acid induced-intracellular lipid accumulation and enhances autophagy in NIT-1 pancreatic β cells through AMPK activation. Journal of ethnopharmacology 32 25510732
2007 Glucose regulated proteins 78 protects insulinoma cells (NIT-1) from death induced by streptozotocin, cytokines or cytotoxic T lymphocytes. The international journal of biochemistry & cell biology 32 17689130
2003 Nuclear factor-kappaB translocation mediates double-stranded ribonucleic acid-induced NIT-1 beta-cell apoptosis and up-regulates caspase-12 and tumor necrosis factor receptor-associated ligand (TRAIL). Endocrinology 31 12960048
1984 In vitro reconstitution of nitrate reductase activity of the Neurospora crassa mutant nit-1: specific incorporation of molybdopterin. Archives of biochemistry and biophysics 31 6237611
1998 Structural analysis of the nit2/nit1/nit3 gene cluster encoding nitrilases, enzymes catalyzing the terminal activation step in indole-acetic acid biosynthesis in Arabidopsis thaliana. Plant molecular biology 30 9484465
2010 Suppression of NADPH oxidase 2 substantially restores glucose-induced dysfunction of pancreatic NIT-1 cells. The FEBS journal 28 21073655
2021 The synergistic protection of EGCG and quercetin against streptozotocin (STZ)-induced NIT-1 pancreatic β cell damage via upregulation of BCL-2 expression by miR-16-5p. The Journal of nutritional biochemistry 27 34051305
2013 Vanadium compounds modulate PPARγ activity primarily by increasing PPARγ protein levels in mouse insulinoma NIT-1 cells. Metallomics : integrated biometal science 27 23456093
2012 Effects of sesamin on streptozotocin (STZ)-induced NIT-1 pancreatic β-cell damage. International journal of molecular sciences 27 23443130
1973 In vitro formation of nitrate reductase using extracts of the nitrate reductase mutant of Neurospora crassa, nit-1, and Rhodospirillum rubrum. Journal of bacteriology 25 4270447
2018 NIT1 suppresses tumour proliferation by activating the TGFβ1-Smad2/3 signalling pathway in colorectal cancer. Cell death & disease 23 29449642
2014 Effects of berberine and cinnamic acid on palmitic acid-induced intracellular triglyceride accumulation in NIT-1 pancreatic β cells. Chinese journal of integrative medicine 23 25491540
1997 Protection of NIT-1 pancreatic beta-cells from immune attack by inhibition of NF-kappaB. Journal of autoimmunity 23 9218757
2009 Nit1 and Fhit tumor suppressor activities are additive. Journal of cellular biochemistry 21 19479888
1999 Minute oxidative stress is sufficient to induce apoptotic death of NIT-1 insulinoma cells. APMIS : acta pathologica, microbiologica, et immunologica Scandinavica 21 10515125
2005 The NIT1 promoter allows inducible and reversible silencing of centrin in Chlamydomonas reinhardtii. Eukaryotic cell 20 16278463
2013 Antioxidant effect of mogrosides against oxidative stress induced by palmitic acid in mouse insulinoma NIT-1 cells. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 19 24270904
2012 Bradykinin prevents the apoptosis of NIT-1 cells induced by TNF-α via the PI3K/Akt and MAPK signaling pathways. International journal of molecular medicine 19 22367460
2019 The metabolite repair enzyme Nit1 is a dual-targeted amidase that disposes of damaged glutathione in Arabidopsis. The Biochemical journal 17 30692244
2016 Genomic analysis of Bacillus subtilis lytic bacteriophage ϕNIT1 capable of obstructing natto fermentation carrying genes for the capsule-lytic soluble enzymes poly-γ-glutamate hydrolase and levanase. Bioscience, biotechnology, and biochemistry 16 27885938
2013 Studies on recombination processes in two Chlamydomonas reinhardtii endogenous genes, NIT1 and ARG7. Protist 15 23792631
2022 Nitrilases NIT1/2/3 Positively Regulate Flowering by Inhibiting MAF4 Expression in Arabidopsis. Frontiers in plant science 14 35665187
2011 Erythropoietin protects pancreatic β-cell line NIT-1 cells against cytokine-induced apoptosis via phosphatidylinositol 3-kinase/Akt signaling. Endocrine research 14 21226565
2008 Transplantation of NIT-1 cells expressing pD-L1 for treatment of streptozotocin-induced diabetes. Transplantation 14 19077895
2002 Cell surface trafficking of Fas in NIT-1 cells and dissection of surface and total Fas expression. Biochemical and biophysical research communications 14 11779190
1995 Expression of an insulin/interleukin-1 receptor antagonist hybrid gene in insulin-producing cell lines (HIT-T15 and NIT-1) confers resistance against interleukin-1-induced nitric oxide production. The Journal of clinical investigation 14 7706480
2012 The protective effect of MT-α-glucan against streptozotocin (STZ)-induced NIT-1 pancreatic β-cell damage. Carbohydrate polymers 13 23399148
2016 The Different Effects of Atorvastatin and Pravastatin on Cell Death and PARP Activity in Pancreatic NIT-1 Cells. Journal of diabetes research 11 28004006
2008 Impact of cytokine- and FasL-induced apoptosis in the beta-cell line NIT-1. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 9 18975252
2017 The PI3K/Akt1-FoxO1 Translocation Pathway Mediates EXf Effects on NIT-1 Cell Survival. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association 8 28895639
2009 Mammalian nitrilase 1 homologue Nit1 is a negative regulator in T cells. International immunology 8 19395373
2007 [Effect of berberine on insulin secretion and glucokinase activity of NIT-1 cells]. Yao xue xue bao = Acta pharmaceutica Sinica 8 18229609
2024 Metformin enhances METTL14-Mediated m6A methylation to alleviate NIT-1 cells apoptosis induced by hydrogen peroxide. Heliyon 7 38312705
2021 MicroRNA-7a inhibits Isl1 expression to regulate insulin secretion by targeting Raf1 and Mapkap1 in NIT-1 cells. In vitro cellular & developmental biology. Animal 7 34713362
2011 Crystal structure of bacteriophage ϕNIT1 zinc peptidase PghP that hydrolyzes γ-glutamyl linkage of bacterial poly-γ-glutamate. Proteins 7 22105902
2009 The effects of alginate encapsulation on NIT-1 insulinoma cells: viability, growth and insulin secretion. In vivo (Athens, Greece) 7 20023235
2008 Dominance of cytokine- over FasL-induced impairment of the mitochondrial transmembrane potential (Deltapsim) in the pancreatic beta-cell line NIT-1. Diabetes & vascular disease research 7 18777493
2004 Fas ligand down-regulates cytokine-induced Fas receptor expression on insulinoma (NIT-1), but not islet cells, from autoimmune nonobese diabetic mice. Endocrinology 7 15033908
2019 Danzhi Jiangtang Capsule Mediates NIT-1 Insulinoma Cell Proliferation and Apoptosis by GLP-1/Akt Signaling Pathway. Evidence-based complementary and alternative medicine : eCAM 6 31467576
2001 Immature granules are not major sites for segregation of constitutively secreted granule content proteins in NIT-1 insulinoma cells. Biochemical and biophysical research communications 6 11700020
1984 Activation of nit-1 nitrate reductase by W-formate dehydrogenase. Biochemical and biophysical research communications 6 6234890
2024 Bi-allelic NIT1 variants cause a brain small vessel disease characterized by movement disorders, massively dilated perivascular spaces, and intracerebral hemorrhage. Genetics in medicine : official journal of the American College of Medical Genetics 5 38430071
2021 Silencing of the tRNA Modification Enzyme Cdkal1 Effects Functional Insulin Synthesis in NIT-1 Cells: tRNALys3 Lacking ms2- (ms2t6A37) is Unable to Establish Sufficient Anticodon:Codon Interactions to Decode the Wobble Codon AAG. Frontiers in molecular biosciences 5 33634165
2018 Sall2 knockdown exacerbates palmitic acid induced dysfunction and apoptosis of pancreatic NIT-1 beta cells. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 5 29783189
2011 Lipopolysaccharide-enhanced early proliferation of insulin secreting NIT-1 cell is associated with nuclear factor-kappaB- mediated inhibition of caspase 3 cleavage. Chinese medical journal 4 22340219
2009 Regulation of adiponectin receptor 2 expression via PPAR-alpha in NIT-1 cells. Endocrine journal 4 19336949
1997 Modulation and detection of IDDM by membrane associated antigens from the islet beta cell line NIT-1. Journal of autoimmunity 4 9080297
2025 CEPR1 regulates Arabidopsis thaliana root architecture by modulating auxin production via NIT1. The Plant journal : for cell and molecular biology 2 40664202
2024 Nitrilases NIT1/2/3 Positively Regulate Resistance to Pseudomonas syringae pv. tomato DC3000 Through Glucosinolate Metabolism in Arabidopsis. International journal of molecular sciences 2 39684605
2023 The Rosetta Stone Hypothesis-Based Interaction of the Tumor Suppressor Proteins Nit1 and Fhit. Cells 2 36766695
2013 Structural and functional characterization of the Colletotrichum lindemuthianum nit1 gene, which encodes a nitrate eductase enzyme. Genetics and molecular research : GMR 2 23420367
2024 Exploring the potential of semi-synthetic Swertiamarin analogues for GLUT facilitation and insulin secretion in NIT-1 cell lines: a molecular docking and in-vitro study. Natural product research 1 38619018
2025 Nit1 is upregulated in non-small cell lung cancer and promotes cancer cell proliferation and invasion and regulates EMT-related molecules and cyclins. Journal of Cancer 0 40740246
2025 Identification of the function of the metabolite repair enzyme Nit1: the story of a collaboration with Arthur Cooper. Analytical biochemistry 0 41390003
2024 The Counteracting Effects of Ang II and Ang-(1-7) on the Function andGrowth of Insulin-secreting NIT-1 Cells. Current diabetes reviews 0 38173074
2009 Transplantation of NIT-1 cells with ectopic FADDdel-GFP expression for treatment of streptozotocin-induced diabetes. Autoimmunity 0 19811259
2008 [Effect of supplemented Taoren Chengqi decoction on NIT-1, a pancreatic beta-cell from a transgenic NOD/Lt mouse]. Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 0 18837325
2005 [Oxidative damage and apoptosis in NIT-1 cells induced by ethanol]. Wei sheng yan jiu = Journal of hygiene research 0 16111037
2005 [Construction and identification of procaryotic expression vector of human NIT1 gene]. Zhongguo fei ai za zhi = Chinese journal of lung cancer 0 21189170