| Necroptosis as an alternative form of programmed cell death. | |
| | |
MedLine Citation:
|
PMID: 20045303 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The family of death receptors plays a critical role in regulating cell number and eliminating harmful or virally infected cells. Agonistic stimulation of death receptors is known to lead two alternative cell fates by either activating NF-kappaB to promote cell survival or inducing apoptosis to lead to cell death; and now a third pathway, termed necroptosis or programmed necrosis has been identified. Interestingly, a death-domain containing kinase, RIP1, is involved in mediating all three pathways, with its kinase activity specifically involved in regulating necroptosis. The availability of necrostatin-1, a specific inhibitor of RIP1 kinase, made it possible to dissect the distinct functional domains of RIP1. Recent genome-wide siRNA screens have identified multiple players of necroptosis that may interact with and/or regulate RIP1 kinase and mediate the signaling pathway and execution of necroptosis. Necroptosis and necrostatins provide an exciting new opportunity for developing new treatments for multiple human diseases involving necrosis and inflammation. |
| | |
Authors:
|
Dana E Christofferson; Junying Yuan |
Related Documents
:
|
10737593 - Interaction among mitochondria, mitogen-activated protein kinases, and nuclear factor-k... 20300203 - The ikk complex, a central regulator of nf-kappab activation. 20558733 - Rhamm promotes interphase microtubule instability and mitotic spindle integrity through... |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2010-01-04 |
Journal Detail:
|
Title: Current opinion in cell biology Volume: 22 ISSN: 1879-0410 ISO Abbreviation: Curr. Opin. Cell Biol. Publication Date: 2010 Apr |
Date Detail:
|
Created Date: 2010-04-12 Completed Date: 2010-06-23 Revised Date: 2011-07-27 |
Medline Journal Info:
|
Nlm Unique ID: 8913428 Medline TA: Curr Opin Cell Biol Country: England |
Other Details:
|
Languages: eng Pagination: 263-8 Citation Subset: IM |
Copyright Information:
|
Copyright 2009 Elsevier Ltd. All rights reserved. |
Affiliation:
|
Department of Cell Biology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115, United States. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Apoptosis* Humans Models, Biological Necrosis / pathology* Receptor-Interacting Protein Serine-Threonine Kinases / metabolism Ubiquitination |
| Grant Support | |
ID/Acronym/Agency:
|
DP1 OD000580-05/OD/NIH HHS; R37 AG012859-16/AG/NIA NIH HHS; R37-AG012859/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
|
EC 2.7.11.1/Receptor-Interacting Protein Serine-Threonine Kinases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Connecting autophagy to senescence in pathophysiology.
Next Document: Cytoprotective roles for autophagy.