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ToolsMcFarlane, Shona M., Pashmi, Ghazaleh, Connell, Michelle C., Littlejohn, Alison F., Tucker, Steven J., Vandenabeele, Peter and MacEwan, David J. (2002) Differential activation of nuclear factor-kappa B by tumour necrosis factor receptor subtypes. TNFR1 predominates whereas TNFR2 activates transcription poorly. FEBS Letters, 515 (1-3). pp. 119-126. ISSN 0014-5793
Full text not available from this repository.Abstract
Tumour necrosis factor-alpha (TNF-alpha) signals though two receptors, TNFR1 and TNFR2. TNFR1 has a role in cytotoxicity, whereas TNFR2 regulates death responses or proliferation. TNF activates pro-inflammatory transcription factor nuclear factor-kappaB (NF-kappaB) by uncertain signalling mechanisms. Here we report the contribution of each TNFR towards the NF-kappaB activation processes. In human cells expressing endogenous or exogenous TNFR2, in addition to TNFR1, we found both TNFRs capable of activating NF-kappaB as measured by IkappaBalpha (inhibitor of NF-kappaB) degradation, electrophorefic mobility shift assay and NF-kappaB gene reporter assays. TNFR2 activation did not degrade IkappaBbeta. However, TNF-effects on NF-kappaB activation occurred predominantly through TNFR1, with TNFR2 activating the transcription factor poorly. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | cell-death,cytotoxicity,induction,tumour,proliferation,signal transduction,signaling pathway,kinase,apoptosis,cytokine,receptor,subtype,identification,domain,kinase,alpha |
| Faculty \ School: | Faculty of Science > School of Pharmacy |
| Depositing User: | Rachel Smith |
| Date Deposited: | 23 May 2011 10:05 |
| Last Modified: | 24 Oct 2022 03:21 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/31042 |
| DOI: | 10.1016/S0014-5793(02)02450-X |
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