TCR-mediated Erk activation does not depend on Sos and Grb2 in peripheral human T cells |
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Authors: | Warnecke Nicole Poltorak Mateusz Kowtharapu Bhavani S Arndt Boerge Stone James C Schraven Burkhart Simeoni Luca |
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Institution: | Institute of Molecular and Clinical Immunology, Otto-von-Guericke University, Leipziger Strasse 44, Magdeburg 39120, Germany. |
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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. |
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Keywords: | T cells Sos Grb2 RasGRP1 Erk |
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