TCR-mediated Erk activation does not depend on Sos and Grb2 in peripheral human T cells.

Warnecke, Nicole; Poltorak, Mateusz; Kowtharapu, Bhavani S; Arndt, Boerge; Stone, James C; Schraven, Burkhart; Simeoni, Luca

dc.contributor.author	Warnecke, Nicole
dc.contributor.author	Poltorak, Mateusz
dc.contributor.author	Kowtharapu, Bhavani S
dc.contributor.author	Arndt, Boerge
dc.contributor.author	Stone, James C
dc.contributor.author	Schraven, Burkhart
dc.contributor.author	Simeoni, Luca
dc.date.accessioned	2012-07-13T09:44:08Z
dc.date.available	2012-07-13T09:44:08Z
dc.date.issued	2012-04
dc.identifier.citation	TCR-mediated Erk activation does not depend on Sos and Grb2 in peripheral human T cells. 2012, 13 (4):386-91 EMBO Rep.	en_GB
dc.identifier.issn	1469-3178
dc.identifier.pmid	22344067
dc.identifier.doi	10.1038/embor.2012.17
dc.identifier.uri	http://hdl.handle.net/10033/233572
dc.description.abstract	Sos proteins are ubiquitously expressed activators of Ras. Lymphoid cells also express RasGRP1, another Ras activator. Sos and RasGRP1 are thought to cooperatively control full Ras activation upon T-cell receptor triggering. Using RNA interference, we evaluated whether this mechanism operates in primary human T cells. We found that T-cell antigen receptor (TCR)-mediated Erk activation requires RasGRP1, but not Grb2/Sos. Conversely, Grb2/Sos—but not RasGRP1—are required for IL2-mediated Erk activation. Thus, RasGRP1 and Grb2/Sos are insulators of signals that lead to Ras activation induced by different stimuli, rather than cooperating downstream of the TCR.
dc.language.iso	en	en
dc.rights	Archived with thanks to EMBO reports	en_GB
dc.title	TCR-mediated Erk activation does not depend on Sos and Grb2 in peripheral human T cells.	en
dc.type	Article	en
dc.contributor.department	Institute of Molecular and Clinical Immunology, Otto-von-Guericke University, Leipziger Strasse 44, Magdeburg 39120, Germany.	en_GB
dc.identifier.journal	EMBO reports	en_GB
refterms.dateFOA	2012-11-15T00:00:00Z
html.description.abstract	Sos proteins are ubiquitously expressed activators of Ras. Lymphoid cells also express RasGRP1, another Ras activator. Sos and RasGRP1 are thought to cooperatively control full Ras activation upon T-cell receptor triggering. Using RNA interference, we evaluated whether this mechanism operates in primary human T cells. We found that T-cell antigen receptor (TCR)-mediated Erk activation requires RasGRP1, but not Grb2/Sos. Conversely, Grb2/Sos—but not RasGRP1—are required for IL2-mediated Erk activation. Thus, RasGRP1 and Grb2/Sos are insulators of signals that lead to Ras activation induced by different stimuli, rather than cooperating downstream of the TCR.