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Cleavage of Notch1 by Granzyme B Disables Its Transcriptional Activity.
MedLine Citation:
PMID:  21548883     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Granzyme-mediated cell death is the main pathway for cytotoxic lymphocytes to kill virus-infected and tumor cells. A major player in this process is granzyme B (GrB), which triggers apoptosis in both caspase-dependent and caspase-independent manners. 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. We confirmed that Notch1 is a direct and caspase-independent substrate of GrB. We demonstrate that GrB cleaved the intracellular Notch1 domain at least at two distinct aspartic acids D1860 and D1961. Granzyme B 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, likely resulting in anti-cellular proliferation and cell death signals.
Authors:
Geert van Tetering; Niels Bovenschen; Jan Meeldijk; Paul J van Diest; Marc Vooijs
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-6
Journal Detail:
Title:  The Biochemical journal     Volume:  -     ISSN:  1470-8728     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-5-9     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2984726R     Medline TA:  Biochem J     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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