Q6 Which of the outcomes could potentially result if a mutation in the gene encoding the Go subunit eliminates its GTPaseactivity? Choose three outcomes.G& would be ineffective as a signal molecule (that is, it could not activate other proteins).The rate of GTP hydrolysis would increase.The concentration of cAMP in the cell would be continuously elevated.The cell would be unresponsive to molecules that act via cAMP.Go would be activated for an extended period.The signaling pathway could be activated for an extended period, possibly resulting in undesirable cell proliferation.

Heterotrimeric G protein is a complex comprised of 3 protein subunits;, and . They are often…

Answered: Which of the outcomes could potentially…

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter4: Principles Of Neural And Hormonal Communication

Section: Chapter Questions

Problem 5TAHL

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What distinguishes a steroid receptor from a receptor tyrosine kinase receptor or a G-protein-coupled receptor?
Second-messenger systems ultimately bring about the desired cell response by inducing a change in the shape and function of particular designated intracellular proteins. (True or false?)
Activation of certain GPCRs triggers an intracellular signaling mechanism that involves activation of adenlyl cyclase and an increase of cAMP. Which of the following statements best describes the the events that follow such a cAMP increase? a.) The cAMP increase leads to activation of protein kinase C. b.) The cAMP increase leads to activation of the release of the gamma subunit from the GPCR. c.) The cAMP increase leads to activation of protein kinase A.
You are studying a drug that affects a cAMP signalling pathway that is normally initiated when a signalling molecule binds to a G-protein coupled receptor. You determine that the drug prevents the hydrolysis of GTP bound to G-proteins in this pathway. Describe the impact, if any, that this drug would have on the G-protein coupled receptor (GPCR), assuming that the pathway has been activated by the presence of the signalling molecule (first messenger). Include an explanation for your response.
The G protein coupled receptor (GPCR) pathway elicits diverse intracellular responses in different cells. The basic steps of GPCR signaling are outlined in this diagram. Which of the following statements correctly describes the process of GPCR signaling? The GPCR activation is reversible after the signal of the ligand diminishes. The membrane-embedded enzyme uses GTP as a secondary messenger to initiate gene expression. The ligand attaches to both the GPCR and the membrane-embedded enzyme to activate the GPCR pathway. The ligand-bound GPCR sends a GTP molecule to an enzyme in the membrane and switches it into an active state.
Suppose that a G protein undergoes a mutation that allows the exchange of bound GTP for GDP to occur in the absence of G protein binding to a receptor. How might this mutation affect signaling involving a GPCR? Which subunit of the G protein is most likely affected by the mutation?
What is meant by intrinsic GTPase activity? Exchange of GDP for GTP on the a-subunit of the G protein Inhibition of GBCR receptor activity Activation of Adenylyl Cyclades Breakdown of cAMP by phosphodiesterase Spontaneous hydrolysis of GTP on the a-subunit of the G-protein
Dopamine, epinephrine (or norepinephrine) and histamine are important neurotransmitter agonists. When these ligands interact with their cellular receptors, how do they mainly elicit their responses? Choose the correct answer(s) and explain why. a) Activate adenylyl cyclase directly, leading to increased intracellular cAMP levels b) Activate phospholipase C c)Induce or inhibit synthesis of ligand specific intracellular proteins d) Open or close ligand gated ion channels e) Regulate intracellular second messengers through G-protein-coupled receptors
If you have a protein kinase that is regulated by both small molecule inhibitors as well as by phosphorylation, and is part of a cooperative enzyme complex that works as part of a larger pathway involving kinase and GTPase proteins please explain where on this protein regulation could occur, how different types of inhibition could control the function of the protein as well as the function of the complex, and how the protein could regulate other proteins. (This question was previously answered but it was answered incompletely mentioning an herbicide developed in the 1950's. Apparently, it was a plagiarized excerpt from an NCBI article. This is a repost for a full and complete answer. Thank you so much for your help! :) )
Two protein kinases, barley kinase and hops kinase, function sequentially in an intracellular signaling pathway. If either kinase contains a mutation that permanently inactivates it, no response is seen in cells when an extracellular signal is received. A mutation that permanently activates barley results in a response even when there is no extracellular signal. You characterize a double mutant in which hops has the inactivating mutation and barley has the activating mutation. You observe that a response is seen in the double mutants even in the absence of an extracellular signal. In the normal signaling pathway, does barley phosphorylate hops or does hops phosphorylate barley? Briefly explain your answer.
When insulin binds to its receptor, a conformational change occurs that results in auto phosphorylation of the receptor on a specific Tyr residues. In the next step of the signaling pathway, an adaptor protein called IRS-1(insulin receptor substrate-1) docks with the phosphorylated receptor. This step is essential for the downstream activation of several kinases including Alk, also known as protein B as well as protein C kinase and GSK-3. Protein kinase 3 is involved in mobilizing GLUT 4 glucose transporters to the plasma membrane and GSK-3 phosphorylates glycogen sunthase. What would be the effects of a mammalian organism over expressing IRS-1 were also deficient in muscle GAK-3? Would this deficiency be lethal ?
Compare and contrast GPCR and RTK signaling. What role does GTP play in each? What role does phosphorylation play? How is each signal differently amplified? How do these two signaling types compare to steroid signaling with respect to gene activation?

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