CUSTOM BIOLOGY
19th Edition
ISBN: 9781323945490
Author: Urry
Publisher: Pearson Custom Publishing
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Textbook Question
Chapter 11.2, Problem 2CC
WHAT IF? → What would the effect be if a cell made defective receptor tyrosine kinase proteins that were unable to dimerize?
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Pay close attention to the information related to figure 3.14a and the structure of the PKA catalytic site in this figure.
In a few well-written sentences, propose the following:
A mutation that would result in PKA becoming a dead kinase*.
A mutation that would result in PKA becoming a constitutively active** kinase.
Chapter 11 Solutions
CUSTOM BIOLOGY
Ch. 11.1 - Explain how signaling is involved in ensuring that...Ch. 11.1 - In liver cells, glycogen Phosphorylase acts in...Ch. 11.1 - Prob. 3CCCh. 11.2 - Prob. 1CCCh. 11.2 - WHAT IF? What would the effect be if a cell made...Ch. 11.2 - MAKE CONNECTIONS How is ligand binding similar to...Ch. 11.3 - What is a protein kinase, and what is its role in...Ch. 11.3 - When a signal transduction pathway involves a...Ch. 11.3 - What is the actual signal that is being transduced...Ch. 11.3 - WHAT IF? If you exposed a cell to a ligand that...
Ch. 11.4 - How can a targct cell's response to a single...Ch. 11.4 - WHAT IF? If two cells have different scaffolding...Ch. 11.4 - Prob. 3CCCh. 11.4 - Prob. 4CCCh. 11.5 - Give an example of apoptosis during embryonic...Ch. 11.5 - WH AT IF? If apoptosis occurred when it should...Ch. 11 - What determines whether a cell responds to a...Ch. 11 - How are the structures of a GPCR and an RTK...Ch. 11 - What is the difference between a protein kinase...Ch. 11 - What mechanisms in the cell terminale its response...Ch. 11 - What is an explanation for the similarities...Ch. 11 - Binding of a signaling molecule to which type of...Ch. 11 - The activation of receptor tyrosinc kinases is...Ch. 11 - Lipid-soluble signaling molecules, such as...Ch. 11 - Consider this pathway: epinephrine G...Ch. 11 - Apoptosis involves all but which of the following?...Ch. 11 - Which Observation suggestcd to Sutherland the...Ch. 11 - Prob. 7TYUCh. 11 - DRAW IT Draw the following apoptotic pathway,...Ch. 11 - EVOLUTION CONNECTION Identify the evolutlonary...Ch. 11 - Prob. 10TYUCh. 11 - SCIENCE, TECHNOLOGY, AND SOCIETY The aging process...Ch. 11 - WRITE ABOUT A THEME: ORGANIZATION The properties...Ch. 11 - SYNTHESIZE YOUR KNOWLEDGE There are five basic...
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- More than 500 genes have been identified in the human genome that code for protein kinases. What does such identification imply regarding the role of protein kinases in cellular functions? Explain your answer.arrow_forwardRTK: What would the following double mutations mean for the status of the signaling pathway, and the phosphorylation of MAPKK (MEK)? 1. Ligand is bound to the receptor; MAPK T120A mutation (T120 is normally phosphorylated by MAPKK) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEK 2) Ligand is not bound to the receptor; MAPKKK T132E mutation (T132 is normally phosphorylated by Ras) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEKarrow_forward8 80 wh 가 Vt WI V N Messenger GDP 1 BY G protein Receptor Lumen of endoplasmic reticulum Ca Membrane of endoplasmic reticulum 2 " GDP GTP GTP (5b) Phospholipase C PIP 2 3 IP3 DAG (6c) Calmodulin Protein kinase Protein-P © 2011 Pearson Education, Inc. (4a) 6b Protein kinase C ATP + protein Extracellular fluid (5a) Response in cell (contraction, metabolism, transport) ADP protein- p (6a) Response in cell Response in cell (contraction, secretion) Cytosol Which Ga protein activates phospholipase C? Which secondary messenger opens the ligand gated ion channel? What does a kinase do? What does a phosphatase do?arrow_forward
- 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 GEFarrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, has the highest specificity in binding to the target Protein J?arrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: Describe the relative binding affinities of Ligand A to Protein K and to the active and inactive forms of Protein J. Determine which will Ligand A bind with the highest, medium, and lowest affinity.arrow_forward
- Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, may be expected to be the most potent or have the highest activity against cancer? Explain. b. Which of the ligands, based on the table, may be expected to be least toxic to normal cells? Explain.arrow_forward. which of the following statements about heterotrimetric G proteins and their receptors is incorrect? A: when GTP binds to the alpha subunit of the G protein, the beta-gamma subunit dissociates from the alpha subunit B: G-protein coupled receptors contain nine transmembrane alpha helices C: binding of arrestin causes removal of the receptor from the membrane D: G protein- coupled receptors may be desensitized by serine phosphorylation I had chosen option A and got it wrong. What is the Correct answer and explain how it is. Also, where did i go wrong in choosing option A?arrow_forwardFill in the gaps: For M-Cdk to be activated, inhibitory and activating phosphorylate the mitotic CDK, whilst an activating dephosphorylates the mitotic Cdk. O acetyltranferases, kinase O kinases, acetyltransferase O dehydrogenases, acetyltransferase O phosphatases, acetyltransferase O kinases, phosphatasearrow_forward
- What is the purpose of A kinase–associated proteins (AKAPs)? Describe how AKAPs work in heart muscle cells.arrow_forwardWhat is Anchorage Dependence? Describe the different Cell Junctions in Animal cells. What is the only Cell Junction in Plant cells? Why do Plant cells only have one type of Cell Junction? Explain Cell-Cell signaling involving Signal Transduction and G-Proteins.arrow_forwardMutant tyrosine kinase signaling proteins are implicated in many types of human cancer. Hundreds of millions of dollars are required for the basic research and development of a new drug. Tyrosine kinase inhibitor drugs have been approved for cancer treatments by the U.S. Food and Drug Administration. What do you think would be some of the difficulties of finding these drugs given that similar kinases are active in normal cells? Do you think new medications of this type should be developed through government-sponsored research? Why or why not? If not, what alternatives do you propose?arrow_forward
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