A novel tumor necrosis factor (TNF) family member has been cloned and characterized. This protein, designated TNF-related apoptosis-inducing ligand (TRAIL), consists of 281 and 291 aa in the human and murine forms, respectively, which share 65% aa identity. TRAIL is a type II membrane protein, whose C-terminal extracellular domain shows clear homology to other TNF family members. TRAIL transcripts are detected in a variety of human tissues, most predominantly in spleen, lung, and prostate. The TRAIL gene is located on chromosome 3 at position 3q26, which is not close to any other known TNF ligand family members. Both full-length cell surface expressed TRAIL and picomolar concentrations of soluble TRAIL rapidly induce apoptosis in a wide variety of transformed cell lines of diverse origin.
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rdf:type | |
rdfs:comment |
A novel tumor necrosis factor (TNF) family member has been cloned and characterized. This protein, designated TNF-related apoptosis-inducing ligand (TRAIL), consists of 281 and 291 aa in the human and murine forms, respectively, which share 65% aa identity. TRAIL is a type II membrane protein, whose C-terminal extracellular domain shows clear homology to other TNF family members. TRAIL transcripts are detected in a variety of human tissues, most predominantly in spleen, lung, and prostate. The TRAIL gene is located on chromosome 3 at position 3q26, which is not close to any other known TNF ligand family members. Both full-length cell surface expressed TRAIL and picomolar concentrations of soluble TRAIL rapidly induce apoptosis in a wide variety of transformed cell lines of diverse origin.
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skos:exactMatch | |
uniprot:name |
Immunity
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uniprot:author |
Davis-Smith T.,
Din W.S.,
Goodwin R.G.,
Huang C.-P.,
Nicholl J.K.,
Rauch C.,
Schooley K.,
Smith C.A.,
Smolak P.J.,
Sutherland G.R.,
Wiley S.R.
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uniprot:authorsIncomplete |
true
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uniprot:date |
1995
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uniprot:pages |
673-682
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uniprot:title |
Identification and characterization of a new member of the TNF family that induces apoptosis.
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uniprot:volume |
3
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dc-term:identifier |
doi:10.1016/1074-7613(95)90057-8
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