CEDB20003 Lecture Notes - Lecture 20: S Phase, Brain-Derived Neurotrophic Factor, Blastoma

• School: University of Melbourne
• Department: Cell Biology
• Course: CEDB20003
• Professor: Jenny Gunnerson

Document Summary

Gtpase activating proteins (cid:523)gaps(cid:524) (cid:1372) (cid:1371)hydrolysis of gtp. Hyperactive ras mutants are resistance to gap cancer. Dimerization of rtk(cid:495)s permits inhibition of signaling by a dominant negative receptor. Dimerization is important for rtk to occur. Dimerization leads to auto phosphorylation where the two receptors cross phosphorylate each other. No signal transduction if there is a mutant receptor which doesn(cid:495)t have the tail end to help cross phosphorylate each other. Expression of a dominant negatvie fgf receptor inhibits lens differentiation. Phospholipase c , phosphatidylinositol-(cid:885)(cid:495)-kinase, src how do receptors signal inside the cell they must dimerise and cross phosphorylate the phospho tyrisin acts as binding sites for adapter proteins. Multiple adapter proteins bind to either of the receptors. Multiple phospho tyrisine gives you a lot of different pathwys already have divergence. Binding proteins have homologous phospho-tyrosine binding domains src. Sh3 bind domains on other intracellular proteins domains are called src homology domains identifying the motifs there are 2.