Cellular signaling receptor tyrosine kinase

Figure 24.19. Generic signal transduction pathway involving receptor tyrosine kinase (RTK). An extracellular growth factor signal is conveyed via receptors, GTPases (Ras), kinases, and ultimately to transcription factors that alter gene expression and produce a cellular response.

Figure 1 Ras GTPases function as regulated GDP/GTP molecular switches. Diverse extracellular signals, for example those received by membrane-bound receptors such as G-protein coupled receptors and receptor tyrosine kinases, can cause Ras GTPase activation at the plasma membrane and endomembranes. Receptor-mediated activation of Ras most commonly involves the activation of RasGEFs, which then cause transient activation of Ras. Activated Ras-GTP adopts a conformation that enhances its affinity for transient binding to and activation of downstream effectors (E).A The activated effectors then regulate distinct cytoplasmic signaling networks that control cellular proliferation, differentiation, and survival. Ras signaling is terminated by RasGAP-mediated stimulation of hydrolysis of bound GTP to GDP, which precludes further Ras-effector interaction. Tumor-associated Ras mutant proteins are insensitive to GAP stimulation.

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