title: Regulation of RIP1 kinase signalling at the crossroads of inflammation and cell death.
abstract: Receptor-interacting protein 1 (RIP1) kinase has emerged as a key upstream regulator that controls inflammatory signalling as well as the activation of multiple cell death pathways, including apoptosis and necroptosis. The ability of RIP1 to modulate these key cellular events is tightly controlled by ubiquitylation, deubiquitylation and the interaction of RIP1 with a class of ubiquitin receptors. The modification of RIP1 may thus provide a unique 'ubiquitin code' that determines whether a cell activates nuclear factor-κB (NF-κB) to promote inflammatory signalling or induces cell death by apoptosis or necroptosis. Targeting RIP1 might be a novel therapeutic strategy for the treatment of both acute and chronic human diseases.
authors.affiliation: Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
authors.forename: Dimitry
authors.initials: D
authors.lastname: Ofengeim
authors.forename: Junying
authors.initials: J
authors.lastname: Yuan
mesh_terms: D000818:Animals; D016923:Cell Death / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D008954:Models, Biological; D016328:NF-kappa B / Q000378:metabolism; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; C506249:RIPK1 protein, human; D053422:Receptor-Interacting Protein Serine-Threonine Kinases