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Unformatted text preview: I.e., briefly outline the experiment in Figure 1. 3) What is the significance of the fact that PLCII becomes phophorylated within 30 seconds of EGF treatment? 4) Why does PLCII migrate more slowly in a SDS gel after treatment with EGF (Fig 2)? 5) What evidence indicates that EGF receptor and PLC-II are associated with one another in vivo (Fig 3 and Fig 5)? Do these experiments prove that they interact directly? 6) Does the EGF receptor interact with PLC-II in the absence of EGF (see Fig. 3)? 7) How does the use of tyrphostin allow the authors to argue that phosphorylation of PLC-II upon stimulation of EGF receptor is relevant to cell growth and proliferation (Figs 6, 7, 8, and 9)? 8) Inhibition of the EGF kinase activity with tyrphostin blocked the EGF-induced Ca++ increase in the cytoplasm. What pathway that leads to increase in Ca++ might be failing? 9) What is a mitogen?...
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- Spring '08