RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mo...
RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury
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Author / Creator
Newton, K , Dugger, D L , Maltzman, A , Greve, J M , Hedehus, M , Martin-McNulty, B , Carano, R A D , Cao, T C , van Bruggen, N , Bernstein, L , Lee, W P , Wu, X , DeVoss, J , Zhang, J , Jeet, S , Peng, I , McKenzie, B S , Roose-Girma, M , Caplazi, P , Diehl, L , Webster, J D and Vucic, D
Publisher
London: Nature Publishing Group UK
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English
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London: Nature Publishing Group UK
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Necroptosis is a caspase-independent form of cell death that is triggered by activation of the receptor interacting serine/threonine kinase 3 (RIPK3) and phosphorylation of its pseudokinase substrate mixed lineage kinase-like (MLKL), which then translocates to membranes and promotes cell lysis. Activation of RIPK3 is regulated by the kinase RIPK1....
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Full title
RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury
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TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5072432
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https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5072432
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ISSN
1350-9047
E-ISSN
1476-5403
DOI
10.1038/cdd.2016.46
