| Autor: |
McFarlane SM; Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, AB25 2ZD, Aberdeen, UK., Pashmi G, Connell MC, Littlejohn AF, Tucker SJ, Vandenabeele P, MacEwan DJ |
| Jazyk: |
angličtina |
| Zdroj: |
FEBS letters [FEBS Lett] 2002 Mar 27; Vol. 515 (1-3), pp. 119-26. |
| DOI: |
10.1016/s0014-5793(02)02450-x |
| Abstrakt: |
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, electrophoretic 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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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