Stimulation of p21ras upon T-cell activation

Article Abstract:

The first identification of oncogenes in cancer-causing viruses led to the observation of similar genes, called proto-oncogenes, in normal cells. One such proto-oncogene is ras, which has been identified in a wide range of species. Several related ras genes have been discovered, and although their role in the transformation of normal cells to tumor cells has been widely studied, the physiological function of ras genes in normal healthy cells has remained uncertain. Now it has been shown that the stimulation of T cells through the binding of specific antigen to their receptors involves a rapid activation of p21ras, or the 21-kilodalton protein coded by the ras gene. The activation apparently results from a decrease in the activity of GAP. GAP, or GTPase activating protein, promotes the conversion of GTP to GDP on the p21ras protein. Therefore, most of the guanine nucleotides on p21ras are in the form of GDP rather than GTP. When the T cells are stimulated, the activity of GAP is reduced, and GTP replaces GDP as the predominant nucleotide. The researchers suggest that this change in p21ras results from the activity of protein kinase C. They were able to observe that direct stimulation of protein kinase C produced results similar to those observed by stimulation of the T-cell receptor. They were unable to demonstrate any direct modification of GAP by protein kinase C, however, and propose that a GTP-exchange protein might be the direct target of the protein kinase C activity. This research is the first direct demonstration of the involvement of p21ras in normal cellular processes. It is clear, however, that further research will be necessary to work out the details. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Cancer, Cancer genetics, Cell receptors, T cells, Proto-oncogenes

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Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB

Article Abstract:

The role of phosphatidylinositol-3-kinase (PI(3)K) in the cellular signal transduction pathway that promotes apoptosis in fibroblasts was analyzed in rodent cells during c-Myc-induced apoptosis. Expression of a constitutively active PI(3)K in rodent cells inhibited c-Myc-induced apoptosis via Ras activation PKB/Akt downstream protein kinase activators. Furthermore, inhibition of apoptosis indicated the presence of a putative anti-apoptotic pathway from Ras to PI(3)K and PKB/Akt.

Cell death, Cellular signal transduction

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Direct interaction of Ras and the amino-terminal region of Raf-1 in vitro

Article Abstract:

Raf appears to be a direct target enzyme of Ras. If so, it is the first such effector to be identified. The regulatory region of p74(c-raf-1) expressed as a GST fusion protein binds directly to Ras with a high affinity of 50 nM, when Ras is in the active (GTP-bound) state. Evidence that Ras can control the kinase activity of full-length Raf would prove the connection. This research does not eliminate the possibility of other effectors of Ras.

Research, Growth factors, Proteins

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