Publication Date:
2016-04-02
Description:
Until recently, programmed cell death was conceived of as a single set of molecular pathways. We now know of several distinct sets of death-inducing mechanisms that lead to differing cell-death processes. In one of them--apoptosis--the dying cell affects others minimally. In contrast, programmed necrotic cell death causes release of immunostimulatory intracellular components after cell-membrane rupture. Defining the in vivo relevance of necrotic death is hampered because the molecules initiating it [such as receptor-interacting protein kinase-1 (RIPK1), RIPK3, or caspase-1] also serve other functions. Proteins that participate in late events in two forms of programmed necrosis [mixed lineage kinase domain-like protein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bringing us closer to identifying molecules that strictly serve in death mediation, thereby providing probes for better assessing its role in inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wallach, David -- Kang, Tae-Bong -- Dillon, Christopher P -- Green, Douglas R -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):aaf2154. doi: 10.1126/science.aaf2154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomolecular Sciences, The Weizmann Institute of Science, 76100 Rehovot, Israel. d.wallach@weizmann.ac.il douglas.green@stjude.org. ; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chung-Ju 380-701, Korea. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. d.wallach@weizmann.ac.il douglas.green@stjude.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034377" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Apoptosis
;
Caspase 1/metabolism
;
Cytokines/metabolism
;
Humans
;
Inflammation/*metabolism/*pathology
;
Necrosis/pathology
;
Neoplasm Proteins/metabolism
;
Protein Kinases/metabolism
;
Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
