Consider a KDEL receptor that has been altered to prevent its cargo (proteins with a KDEL sequence) from dissociating (releasing) within the ER lumen. What would the result of this mutation be?
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Consider a KDEL receptor that has been altered to prevent its cargo (proteins with a KDEL sequence) from dissociating (releasing) within the ER lumen. What would the result of this mutation be?
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- Would the following alterations to Src be oncogenic? Explain. (a) The deletion or inactivation of the SH3 domain. (b) The mutation of Tyr 416 to Phe.What do the cytoplasmic domain of a G protein-coupled receptor and the adaptor protein in the RTK pathway have in common?How do RER and SER differ from one another in terms of structure and function? List the processes in which the ER is involved.
- Continuous exposure of a Gαs protein coupled receptor to its ligand leads to a phenomenon known as desensitization. Describe several molecular mechanisms for receptor desensitization. How can a receptor be reset to its original sensitized state? What effect would a mutant receptor lacking serine or threonine phosphorylation sites have on a cell?Serotonin is a neurotransmitter that is a small, soluble molecule. P11 (a small protein) is required for transport of serotonin receptors to the cell surface. Assume for this problem that p11 affects transport of serotonin receptors only, and that it does not affect transport of any other proteins (a simplification). Depressed people seem to have low levels of p11; treatments that improve mood increase the expression of the p11 gene. NSAIDs (aspirin, ibuprofen, etc.) seem to decrease expression of p11. SSRIs (selective serotonin reuptake inhibitors) decrease re-uptake of serotonin at synapses. Some depressed patients are helped by SSRIs, but some are not. Explain both parts of B. B-1. The results indicate that depression can be caused by levels of serotonin receptors that are (higher than normal) (lower than normal) (neither – no evidence here for any effect on depression) (higher or lower but can't tell which). B-2. If a depressed person does not respond to SSRIs, the person…GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEF
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сокSee figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.Binding of a ligand (like TGFA) to a receptor tyrosine kinase (RTK) causes all of the following except (can use cell): OA. Dimerization of the receptor B. Auto-phosphorylation of the receptor O C. Activation of Ras through an interction with GRB2 (an adaptor) and SOS (a GEF) proteins. O D. Activation of heterotrimeric G proteins
- An SH2-containing protein contains a mutation that changes its binding pocket such that tyrosine and phosphotyrosine bind with equal affinity. As a result, MEK activity: does not change with receptor dimerization and transautophosphorylation decreases due to changes in Raf activation increases with ligand binding-induced dimerization decreases due to allosteric inhibition of SH2-domain bindingWhich of the following would you expect to happen if amino acids 579 to 582 (YIYV) in the PDGF-Beta receptor were exchanged with amino acids 992 to 995 (YLIP) from the EGF receptor to give PDGF (YLIP) and EGF (YIYV) (Select all that apply)? (A) PDGF-B receptor Src I NCK-B SHP2 PLC-y P 579 P 581 YIYV PI3KY P 740 YMDM NCK-a P 751 YVPM P 771 YMAP GAP P 1009 YTAV P 1021 YIIP (B) POE 845 YHAE 992 YLIP 1045 YSSD 1068 YINQ 1086 YHNK 1148 YQQD 1173 YLRV P P P P P P P EGF receptor STAT3/5 PLC-y Shc Cbl JAK2 Grb2 STAT3/5 Shc SHP1 PTP1You decide to investigate cell signaling of a pair of newly identified GPCRs, GPCR-W and GPCR-Z. Each binds the same ligand, but activates different downstream heterotrimeric G-proteins that act on adenylyl cyclase. You discover that ligand binding has opposite effects on adenylyl cyclase activity for each receptor. GPCR-W causes an increase in adenylyl cyclase activity, while GPCR-Z causes a decrease in adenylyl cyclase activity. You obtain a cell line expressing GPCR-W, GPCR-Z, the relevant G-proteins, and adenylyl cyclase. There is baseline adenylyl cyclase activity producing a baseline amount of cAMP. You embark on a research project to characterize the following mutations in the components of the signaling pathway. 2. Will each of the following mutations increase or decrease the levels of cAMP inside the cell upon adding the ligand to the cell culture? A mutation in Gi that prevents release of bound GDP. A mutation in Gs that prevents GTP hydrolysis. A mutation in Gi that…