T cell stimulation via the TCR complex (TCR/CD3 complex) results in activation of the guanine nucleotide binding proteins encoded by the ras protooncogenes (p21(ras)). In the present study we show that the activation state of p21(ras) in T lymphocytes can also be controlled by triggering of the CD2 Ag. The activation state of p21(ras) is controlled by GTP levels on p21(ras). In T cells stimulation of protein kinase C is able to induce an accumulation of 'active' p21(ras)-GTP complexes due to an inhibitory effect of protein kinase C stimulation on the intrinsic GTPase activity of p21(ras). The regulatory effect of protein kinase C on p21(ras) GTPase activity appears to be mediated via regulation of GAP, the GTPase activating protein of p21(ras). In the present report, we demonstrate that the TCR/CD3 complex and the CD2 Ag control the accumulation of p21(ras)-GTP complexes via a regulatory effect on p21(ras) GTPase activity. The TCR/CD3 complex and CD2 Ag are also able to control the cellular activity of GAP. These data demonstrate that p21(ras) is part of the signal transduction responses controlled by the CD2 Ag, and reveal that the TCR/CD3 complex and CD2 Ag control the activation state of p21(ras) via a similar mechanism.
|Number of pages||4|
|Journal||Journal of Immunology|
|Publication status||Published - 1 Jun 1991|