ArticleThe Biochemical journal2011
Cleavage of Notch1 by granzyme B disables its transcriptional activity.
Article in The Biochemical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Aberrant intra-epithelial lymphocytes cause enterocyte cell death in refractory celiac disease by CD103-β7-receptor-mediated granzyme-B degranulation which can be restored by etrolizumab.Clinical & translational immunology · 2026Article
- Reassessing granzyme B: unveiling perforin-independent versatility in immune responses and therapeutic potentials.Frontiers in immunology · 2024Review
- Notch signaling functions in noncanonical juxtacrine manner in platelets to amplify thrombogenicity.eLife · 2022Article
- Review
- The Dual Roles of Human γδ T Cells: Anti-Tumor or Tumor-Promoting.Frontiers in immunology · 2020Review
- Nonapoptotic and extracellular activity of granzyme B mediates resistance to regulatory T cell (Treg) suppression by HLA-DR-CD25hiCD127lo Tregs in multiple sclerosis and in response to IL-6.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Regulated proteolysis of NOTCH2 and NOTCH3 receptors by ADAM10 and presenilins.Molecular and cellular biology · 2014Article
- Improved HSC reconstitution and protection from inflammatory stress and chemotherapy in mice lacking granzyme B.The Journal of experimental medicine · 2014Article
- High NOTCH activity induces radiation resistance in non small cell lung cancer.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Granzyme-mediated cell death is the main pathway for cytotoxic lymphocytes to kill virus-infected and tumour cells. A major player in this process is GrB (granzyme B), which triggers apoptosis in both caspase-dependent and caspase-independent pathways. A caspase-independent substrate of GrB is the highly conserved transmembrane receptor Notch1. The GrB cleavage sites in Notch1 and functional consequences of Notch1 cleavage by GrB were unknown. In the present study, we confirmed that Notch1 is a direct and caspase-independent substrate of GrB. We demonstrate that GrB cleaved the intracellular Notch1 domain at least twice at two distinct aspartic acids, Asp1860 and Asp1961. GrB cleavage of Notch1 can occur in all subcellular compartments, during maturation of the receptor, at the membrane, and in the nucleus. GrB also displayed perforin-independent functions by cleaving the extracellular domain of Notch1. Overall, cleavage of Notch1 by GrB resulted in a loss of transcriptional activity, independent of Notch1 activation. We conclude that GrB disables Notch1 function, probably resulting in anti-cellular proliferation and cell death signals.
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What OpenQuestion holds
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.