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RIP3: a molecular switch for necrosis and inflammation

dc.contributor.authorMoriwaki, Kenta
dc.contributor.authorChan, Francis Ka-Ming
dc.date2022-08-11T08:08:31.000
dc.date.accessioned2022-08-23T15:57:47Z
dc.date.available2022-08-23T15:57:47Z
dc.date.issued2013-08-01
dc.date.submitted2015-01-15
dc.identifier.citationGenes Dev. 2013 Aug 1;27(15):1640-9. doi: 10.1101/gad.223321.113. <a href="http://dx.doi.org/10.1101/gad.223321.113">Link to article on publisher's site</a>
dc.identifier.issn0890-9369 (Linking)
dc.identifier.doi10.1101/gad.223321.113
dc.identifier.pmid23913919
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30281
dc.description.abstractThe receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23913919&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsPublisher PDF posted as allowed by the publisher's author rights policy at http://genesdev.cshlp.org/site/misc/terms.xhtml.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subjectAnimals
dc.subjectEmbryonic Development
dc.subjectGene Expression Regulation
dc.subjectHumans
dc.subjectInflammation
dc.subjectNecrosis
dc.subjectNeoplasms
dc.subjectProtein Processing, Post-Translational
dc.subjectReceptor-Interacting Protein Serine-Threonine Kinases
dc.subjectSignal Transduction
dc.subjectFADD
dc.subjectMLKL
dc.subjectPGAM5
dc.subjectRIP1
dc.subjectcaspase 8
dc.subjectinflammation
dc.subjectCellular and Molecular Physiology
dc.subjectDevelopmental Biology
dc.subjectImmunopathology
dc.subjectMolecular Genetics
dc.subjectPathology
dc.titleRIP3: a molecular switch for necrosis and inflammation
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume27
dc.source.issue15
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1533&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/534
dc.identifier.contextkey6532261
refterms.dateFOA2022-08-23T15:57:47Z
html.description.abstract<p>The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.</p>
dc.identifier.submissionpathfaculty_pubs/534
dc.contributor.departmentDepartment of Pathology
dc.source.pages1640-9


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