Biochemistry: The Molecular Basis of Life
6th Edition
ISBN: 9780190209896
Author: Trudy McKee, James R. McKee
Publisher: Oxford University Press
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Chapter 16, Problem 3Q
Summary Introduction
To review:
The sequence of events occurring on the binding of epinephrine, which triggers the synthesis of cAMP and the reason behind the breaking down of cAMP rapidly.
Introduction:
There are certain hormones; the actions of which are mediated by another set of molecules known as the second messenger. Some of the second messengers include cAMP (cyclic adenosine monophosphate), cGMP (cyclic guanosine monophosphate), inositol-phospholipid system, and calcium ions.
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Chapter 16 Solutions
Biochemistry: The Molecular Basis of Life
Ch. 16 - Prob. 1QCh. 16 - Prob. 2QCh. 16 - Prob. 3QCh. 16 - Prob. 4QCh. 16 - Prob. 5QCh. 16 - Prob. 6QCh. 16 - Prob. 7QCh. 16 - Prob. 8QCh. 16 - Prob. 1RQCh. 16 - Prob. 2RQ
Ch. 16 - Prob. 3RQCh. 16 - Prob. 4RQCh. 16 - Prob. 5RQCh. 16 - Prob. 6RQCh. 16 - Prob. 7RQCh. 16 - Prob. 8RQCh. 16 - Prob. 9RQCh. 16 - Prob. 10RQCh. 16 - Prob. 11RQCh. 16 - Prob. 12RQCh. 16 - Prob. 13RQCh. 16 - Prob. 14RQCh. 16 - Prob. 15RQCh. 16 - Prob. 16RQCh. 16 - Prob. 17RQCh. 16 - Prob. 18RQCh. 16 - Prob. 19RQCh. 16 - Prob. 20RQCh. 16 - Prob. 21RQCh. 16 - Prob. 22RQCh. 16 - Prob. 23RQCh. 16 - Prob. 24RQCh. 16 - Prob. 25RQCh. 16 - Prob. 26RQCh. 16 - Prob. 27RQCh. 16 - Prob. 28RQCh. 16 - Prob. 29RQCh. 16 - Prob. 30RQCh. 16 - Prob. 31RQCh. 16 - Prob. 32RQCh. 16 - Prob. 33RQCh. 16 - Prob. 34FBCh. 16 - Prob. 35FBCh. 16 - Prob. 36FBCh. 16 - Prob. 37FBCh. 16 - Prob. 38FBCh. 16 - Prob. 39FBCh. 16 - Prob. 40FBCh. 16 - Prob. 41FBCh. 16 - Prob. 42FBCh. 16 - Prob. 43FBCh. 16 - Prob. 44SACh. 16 - Prob. 45SACh. 16 - Prob. 46SACh. 16 - Prob. 47SACh. 16 - Prob. 48SACh. 16 - Prob. 49TQCh. 16 - Prob. 50TQCh. 16 - Prob. 51TQCh. 16 - Prob. 52TQCh. 16 - Prob. 53TQCh. 16 - Prob. 54TQCh. 16 - Prob. 55TQCh. 16 - Prob. 56TQCh. 16 - Prob. 57TQCh. 16 - Prob. 58TQCh. 16 - Prob. 59TQCh. 16 - Prob. 60TQCh. 16 - Prob. 61TQCh. 16 - Prob. 62TQCh. 16 - Prob. 63TQCh. 16 - Prob. 64TQCh. 16 - Prob. 65TQCh. 16 - Prob. 66TQCh. 16 - Prob. 67TQCh. 16 - Prob. 68TQCh. 16 - Prob. 69TQCh. 16 - Prob. 70TQCh. 16 - Prob. 71TQCh. 16 - Prob. 72TQCh. 16 - Prob. 73TQCh. 16 - Prob. 74TQCh. 16 - Prob. 75TQ
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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- 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 receptorsarrow_forwardThis is a signaling pathway that involves a second messenger: epinephrine → G protein-coupled receptor → G protein → adenylyl cyclase → cAMP. Which one is known as the second messenger?arrow_forwardYou 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.arrow_forward
- The same second messengers are used in many different cells, but the response to second messengers is different in each cell. How is this possible?arrow_forwardname and describe the isoforms of the leptin receptor.arrow_forwardGTPYS is a nonhydrolyzable analog of GTP. Suppose this compound were added to a cell-free system containing active components of an adrenergic signaling system. What consequences would you expect? What would be the effects on CAMP levels? || -0-P-o-P-0-P-o-CH, guanine он он GTPYS -arrow_forward
- Identify which of the following statements is a lie? Select one: a.Diacylglycerol (DAG) and inositol triphosphate (IP3) are byproducts of enzymatic cleaving of PIP2 using phospholipase C while PIP2 formed via enzymatic activity of kinases. b.cAMP is an important second messenger because it serves to activate or inactivate proteins within the cells, especially those cells which their metabolic pathways are regulated by cAMP-dependent kinase (A-kinase). c.Second messengers are molecules that act alternative to signaling molecules to bind to the receptors by altering the structure of cellular proteins.arrow_forwardBriefly describe what is signal amplification process using cAMP as the second messenger for examplearrow_forwardIn the B-acrenergic receptor signaling pathway where desensitization occurs, what protein acts as an effector protein? The activity of the effector protein directly affects the activity of which protein in this pathway? How would the presence of a GAP affect the desensitization process? stimulate it inhibit it have no effect What is the actual mechanism by which desensitization occurs? the receptor is ubiquitinated the hormone is phosphorylated the hormone is degraded the receptor is internalizedarrow_forward
- In a hypothetical cAMP-mediated signal transduction cascade, the GTP-αs/adenylate cyclase interaction following a single hormone–receptor binding event lasts for 2.3 seconds. The catalytic rate (turnover number) for the adenylate cyclase in question is 350 cAMP molecules produced per second. How many cAMP molecules would be produced if five hormone-receptor binding events were to occur before the hormone molecule dissipates in the bloodstream? What is the amplification effect of this step in the signaling pathway?arrow_forwardSuppose 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?arrow_forwardUse the image above to explain how a muscle cell knows when to increases its glucose levels for cell respiration to be ready to fight or flight. (In short form)arrow_forward
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