Publication Date:
1997-04-04
Description:
TRAIL (also known as Apo-2L) is a member of the tumor necrosis factor (TNF) ligand family that rapidly induces apoptosis in a variety of transformed cell lines. The human receptor for TRAIL was found to be an undescribed member of the TNF-receptor family (designated death receptor-4, DR4) that contains a cytoplasmic "death domain" capable of engaging the cell suicide apparatus but not the nuclear factor kappa B pathway in the system studied. Unlike Fas, TNFR-1, and DR3, DR4 could not use FADD to transmit the death signal, suggesting the use of distinct proximal signaling machinery. Thus, the DR4-TRAIL axis defines another receptor-ligand pair involved in regulating cell suicide and tissue homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, G -- O'Rourke, K -- Chinnaiyan, A M -- Gentz, R -- Ebner, R -- Ni, J -- Dixit, V M -- DAMD17-96-1-6085/DA/NIDA NIH HHS/ -- ES08111/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):111-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9082980" target="_blank"〉PubMed〈/a〉
Keywords:
*Adaptor Proteins, Signal Transducing
;
Amino Acid Sequence
;
*Apoptosis
;
Apoptosis Regulatory Proteins
;
Carrier Proteins/metabolism
;
Cell Line
;
Fas-Associated Death Domain Protein
;
Humans
;
Ligands
;
Membrane Glycoproteins/*metabolism
;
Molecular Sequence Data
;
NF-kappa B/metabolism
;
Proteins/metabolism
;
RNA, Messenger/genetics/metabolism
;
Receptor-Interacting Protein Serine-Threonine Kinases
;
Receptors, TNF-Related Apoptosis-Inducing Ligand
;
Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism
;
Recombinant Fusion Proteins/metabolism
;
Signal Transduction
;
TNF Receptor-Associated Factor 1
;
TNF-Related Apoptosis-Inducing Ligand
;
Transfection
;
Tumor Cells, Cultured
;
Tumor Necrosis Factor-alpha/*metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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