Journal
BIOCHEMICAL JOURNAL
Volume 428, Issue -, Pages 429-437Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20091660
Keywords
interferon-alpha receptor (IFN alpha R); Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT pathway); mitogen-activated protein kinase pathway (MAPK pathway); Slp76; T-cell receptor early signalling complex (TCR ESC); Vav
Categories
Funding
- Wellcome Trust [054191]
- U.K. Biotechnology and Biological Sciences Research Council
- Associazione Italiana per la Ricerca sul Cancro
- U.K. Medical Research Council [G0400197]
- MRC [G0400197] Funding Source: UKRI
- Medical Research Council [G0400197] Funding Source: researchfish
Ask authors/readers for more resources
Signalling through the IFN alpha R (interferon-alpha receptor) and TCR (T-cell receptor) in Jurkat T lymphocytes results in distinct immune responses. Despite this both receptors elicit ERK (extracellular-signal-regulated kinase)/MAPK (mitogen-activated protein kinase) phosphorylation. Vav and Slp76 are shown to be required for IFN alpha (interferon-alpha)-stimulated ERK activity. These form a subset of proteins which behave identically on stimulation of both receptors. TCR deletion abrogates IFN alpha R-stimulated MAPK activity, whereas the canonical JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway is unaffected. Thus recruitment of the intact TCR ESC (early signalling complex) is necessary for this downstream MAPK response. Despite using a common ESC, stimulation of the IFN alpha R does not produce the transcriptional response associated with TCR. Up-regulation of the MAPK pathway by IFN alpha R might be important to ensure that the cell responds to only one stimulant.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available