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Mammals II: Downstream of RAS and Actin-Cytoskeleton

  • Chapter
Regulation of the RAS Signaling Network

Abstract

In the two preceding chapters we have learned how (i) RAS is translocated from the cytoplasm to the plasma membrane by its C-terminal farnesylation and a few other covalent modifications, and how (ii) the inactive GDP-bound form of RAS (D-RAS) on the plasma membrane is then converted to the active GTP-bound form (T-RAS) by SOS and a few other GDP/GTP exchange factors (GEFs). In this chapter we will discuss: (i) the role of several distinct RAS GTPase activating proteins (GAPs) in converting the normal T-RAS to D-RAS; (ii) the oncogenic mutants of RAS that are resistant to the action of GAPs; (iii) the role of several distinct effectors of T-RAS in transmitting the oncogenic (or mitogenic) RAS signals further downstream; (iv) the role of actin-cytoskeletal proteins in the regulation of RAS signaling; (v) three G proteins in the Rho family which are involved in the reorganization of the actin-cytoskeleton caused by T-RAS and (vi) the genes whose expression is upregulated or downregulated by T-RAS.

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  1. Hiroshi Maruta
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Maruta, H. (1996). Mammals II: Downstream of RAS and Actin-Cytoskeleton. In: Regulation of the RAS Signaling Network. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1183-6_5

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  • DOI: https://doi.org/10.1007/978-1-4613-1183-6_5

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