ArticleInternational immunology2009
Mammalian nitrilase 1 homologue Nit1 is a negative regulator in T cells.
Article in International immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Gene-level gut microbiome signatures as predictive biomarkers for response to immune checkpoint inhibitors across multiple cancer types.Gut microbes · 2026Article
- 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 · 2025Article
- A Proterozoic microbial origin of extant cyanide-hydrolyzing enzyme diversity.Frontiers in microbiology · 2023Article
- Characterization of the Nit6803 nitrilase homolog from the cyanotrophBiochemistry and biophysics reports · 2021Article
- Nitrilase 1 modulates lung tumor progression in vitro and in vivo.Oncotarget · 2016Article
- A novel role for the tumour suppressor Nitrilase1 modulating the Wnt/β-catenin signalling pathway.Cell discovery · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The mammalian Nit1 protein is homologous to plant and bacterial nitrilases. In flies and worms, Nit1 is fused to the 5' end of Fhit, suggesting that Nit1 may functionally interact with the Fhit pathway. Fhit has been shown to play a role of a tumor suppressor. Somatic loss of Fhit in human tissues is associated with a wide variety of cancers. Deletion of Fhit results in a predisposition to induced and spontaneous tumors in mice. It has been suggested that Nit1 collaborates with Fhit in tumor suppression. Similar to mice lacking Fhit, Nit1-deficient mice are more sensitive to carcinogen-induced tumors. It was previously shown that ectopic expression of Nit1 or Fhit led to caspase activation and apoptosis, and that both proteins may play a role in DNA damage-induced apoptosis. In this study, we analyzed the physiological function of Nit1 in T cells using Nit1-knockout mice. Nit1-deficient T cells can undergo apoptosis induced by DNA damage due to irradiation and chemical treatment. However, apoptosis induced by Fas or Ca(++) signals appeared to be compromised. Additionally, Nit1 deficiency resulted in T cell hyperproliferative responses induced by TCR stimulation. The expressions of T cell activation markers were elevated in Nit1(-/-) T cells. There was a spontaneous cell cycle entry and enhanced cell cycle progression in Nit1(-/-) T cells. These data indicate that Nit1 is a novel negative regulator in primary T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.