TRICK2, a new alternatively spliced receptor that transduces the cytotoxic signal from TRAIL
Autor: | Alison E. Cowper, Xiao-Ning Xu, Gavin R. Screaton, Andrew J. McMichael, Juthathip Mongkolsapaya, John I. Bell |
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Rok vydání: | 1997 |
Předmět: |
Programmed cell death
Molecular Sequence Data Apoptosis Biology Jurkat cells General Biochemistry Genetics and Molecular Biology Fas ligand Receptors Tumor Necrosis Factor TNF-Related Apoptosis-Inducing Ligand 03 medical and health sciences 0302 clinical medicine Cytotoxic T cell Animals Amino Acid Sequence Cloning Molecular Receptor 030304 developmental biology Death domain 0303 health sciences Binding Sites Membrane Glycoproteins Agricultural and Biological Sciences(all) Tumor Necrosis Factor-alpha Biochemistry Genetics and Molecular Biology(all) Fas receptor Molecular biology Cell biology Alternative Splicing Receptors TNF-Related Apoptosis-Inducing Ligand Cell killing 030220 oncology & carcinogenesis COS Cells General Agricultural and Biological Sciences Apoptosis Regulatory Proteins Signal Transduction |
Zdroj: | Current Biology. 7(9):693-696 |
ISSN: | 0960-9822 |
DOI: | 10.1016/s0960-9822(06)00297-1 |
Popis: | A subset of the tumour necrosis factor (TNF) receptor family contain a conserved intracellular motif, the death domain. Engagement of these receptors by their respective ligands initiates a signalling cascade that rapidly leads to cell death by apoptosis. We have cloned a new member of this family, TRICK2, the TRAIL (TNF-related apoptosis-inducing ligand) receptor inducer of cell killing 2. TRICK2 is expressed in a number of cell types, and to particularly high levels in lymphocytes and spleen. Two isoforms of the TRICK2 mRNA are generated by alternative pre-mRNA splicing and differ by a 29 amino-acid extension to the extracellular domain. Overexpression of TRICK2 rapidly induced apoptosis in 293T cells; this induction was dependent upon the presence of the death domain of TRICK2. Using a soluble molecule containing the TRICK2 extracellular domain, we demonstrated that TRICK2, like DR4 [1], is a receptor for TRAIL/APO-2L [2,3] and could inhibit TRAIL-induced killing of lymphocyte lines, such as the Jurkat T-cell line. TRAIL is upregulated upon lymphocyte activation, as is the intensively studied ligand for Fas, FasL [4]. TRAIL and its receptors might therefore provide another system for the regulation of lymphocyte selection and proliferation, as well as providing an additional weapon in the armoury of cytotoxic lymphocytes. |
Databáze: | OpenAIRE |
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