1.Growth factor binding and dimerization Tyrosine kinase domain Growth factor 2. Autophosphorylation Growth factor Grb2 4. Complex assembly Ras GDP SOS (GEF) 3.Binding of adaptor proteins such as Grb2 GDP 5.Guanine nucleotide exchange and activation of Ras GTP Ras GTP Raf 6.Ras binds raf and initiates MAP kinase pathway Is the phosphorylated tyrosine kinase active or inactive? This pathway controls proliferation and cell survival. What is the general type of ligand for tyrosine kinase receptors? What is autophosphorylation?
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- Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway constriction associated with an allergic response. If a mutation in the associated G-protein’s alpha subunit prevented the hydrolysis of GTP how would the allergic response change? More severe allergic response compared to normal G-protein signaling. Less severe allergic response compared to normal G-protein signaling. No allergic response. No change compared to normal G-protein signaling.Please note whether each protein is either a Kinase (K), ATPase (A), GTPase (G), Membrane protein (M). Some proteins may need more than one letter: Dynamin [Choose ] Porin [Choose ] EGF Receptor [Choose ] CD4 [Choose ] P-glycoprotein [Choose ] Rho [Choose ] <3 of 16 Which statement about the IP3 DAG pathway is false? O Diacylglycerol can act as a second messenger. Inositol trisphosphate can act as a second messenger. O Protein kinase C can phosphorylate a wide variety of proteins. O Inositol trisphosphate remains bound to the membrane after phospholipase C catalyzes its formation. Inositol trisphosphate can open ion channels in the membraņes of smooth endoplasmic reticulum, releasing calcium into the cytoplasm.
- Q-Slide #6 Add icons to show what CaMKII does to its substrate proteins Ме СР2 Ca** CP2 Me Glu СВР HAT NMDA-R* CREB Ca** Ca* Ca CAMKII* CAMKII ? The state of the cell shortly after glutamic acid bound its receptor1 of 16 Data from an experiment is shown in the figure below. In the experiment, murine cells were treated with a specific a ligand that activates receptor R. In some cases, the cells were exposed to one of two drugs (X or Y) as well as the ligand or were left untreated (UT). After 30 minutes of treatment, the cells were lysed with a detergent-based buffer to release the soluble membrane, cyosolic and nuclear proteins. Samples from each cell extract were run (in duplicate) by SDS-PAGE (SDS-polyacrylamide gel electrophoresis) in order to separate the proteins by molecular mass (size). The separated proteins were then transferred to a nitrocellulose membrane which was then probed with different antibodies in a western blotting procedure to detect specific phosphorylated proteins or total proteins. If present in the cell extract, these proteins appear as a dark band in the relevant western blot image within the figure. Drug X Drug Y UT Ligand Ligand Ligand Western blotting antibodies…1. EGF interacts with blank to activate the MAP kinase cascade? G protein coupled receptor; receptor Tyrosine kinase; serine/threonine kinase; cdk 2. When a trimetric G protein is activated by gpcf? The three subuni8of the G protein remain tightly associated with each other; the GDP bound to the a subunit is phosphorylated to form bound GTP; it dissociates into a free b subunit as an ay subunit; none
- Which of the following are activated either directly or indirectly by a heterotrimeric G protein subunit (select all that apply)? O IP, receptor O PIP3-dependent protein kinase O Protein Kinase A O Akt O Phospholipase C O Adenylyl cyclase O Phosphoinositide 3-kinaseFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.All of the following are true of integrins except (a) they are receptor proteins (b) they help organize the cytoskeleton (c) they are part of the ECM (d) they are important in cell signaling (e) they are located in the plasma membrane
- Cite evidence supporting a long evolutionary history for cell signaling molecules.11. Explain the role of cytochrome c, Bax/Bac, Fas receptor-ligand, caspases, IGFBP3 in causing apoptosis of cells, based on the figures given below. death ligand cytotoxic cell death receptor plasma membrane -granzyme B executioner caspase 3 initiator caspase 8 procaspases caspase 8 caspase 10 tBid executioner Bid cytochrome c procaspases Apaf-1 apoptosome caspase 9 ICAD lamin death substrates vimentin actin etc. Figure 9.34 The Biology of Cancer (O Garland Science 2014)PDGF 100 PI3K 740 751 PI3K 50 - GAP O771 O GAP PTP P 1009 O PTP protein P-site 1 12 4 5. 6. 7. PI3K 740, 751+ 1021 GAP 771 +] +] PTP 1009 PLC PLCy PLCT 1021 When activated by ligand binding, the PDGF (platelet-derived growth factor) receptor becomes phosphorylated on 5 tyrosine residues (left figure). These phosphorylated tyrosines serve as binding sites for proteins that contain SH2 domains (SH2 domains bind phosphorylated Y). These proteins include phospholipase C-gamma (PLC-gamma), a phosphotyrosine phosphatase (PTP), a Ras GTPase-Activating Protein (GAP), and a phosphotidylinositol 3-Kinase (PI3K). PDGF stimulates several changes in the target cell, one of which is DNA synthesis. To determine which effectors of the PDGF receptor is/are responsible for stimulating DNA synthesis, you construct several mutant forms of the receptor that retain individual or combinations of the phosphorylation sites. You express these in cells and monitor DNA synthesi The results are shown in the right…