Biological Science (7th Edition)
7th Edition
ISBN: 9780134678320
Author: Scott Freeman, Kim Quillin, Lizabeth Allison, Michael Black, Greg Podgorski, Emily Taylor, Jeff Carmichael
Publisher: PEARSON
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Chapter 11, Problem 9TYPSS
Summary Introduction
To review:
The affect of absence of a signal transduction cascade in the processing of steroid hormones: (a) signal amplification, (b) signal regulation, and (c) the cellular response that is possible.
Introduction:
A signaling molecule interacts with the receptor molecule to leave the signal and never enters a cell directly. It is not allowed to enter the cell to prevent a cellular response. The signaling molecules may be hormones, proteins, or other ions. Similarly, steroid hormones such as estrogen and cortisol are signaling molecules, which are hydrophobic in nature. Steroid hormones, like most lipid-soluble signaling molecules, are processed directly.
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Students have asked these 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 receptors
Signaling by soluble extracellular molecules can be classified as endocrine, paracrine, or autocrine. Describe how these three types of cellular signaling differ. Growth hormone is secreted from the pituitary, which is located at the base of the brain and acts through growth hormone receptors located on the liver. Is this an example of endocrine, paracrine, or autocrine signaling? Why?
One such laboratory study investigated the binding of a hormone to three different receptor proteins in the cell membrane. The data collected are shown in the table below:
1) Provide a brief explanation as to why ligand binding to proteins must be a reversible process.
2) Calculate the dissociation constant (Kd) for the hormone binding to each of the three proteins.
3) Which of the proteins demonstrate the tightest/strongest binding of the hormone? Which demonstrates the least tight binding of the hormone? What is the basis for your answer?
Chapter 11 Solutions
Biological Science (7th Edition)
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- 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_forwardPlease identify the incorrect statement about hormone signaling: A) Cystolic receptors bind to hydophobic hormones and transport them into the nucleus where they directly influence protein synthesis. B) Hydropholic hormones cannot pass through the plasma membrane without help. Therefore, there are transport proteins that carry the hydrophillic hormones to the cytosol where it can bind its receptor C) Hydrophilic hormone signalling involves membrane receptors that have the ability to activate adenylyl cyclase, producing cAMP. cAMP then affects the activity of numerous proteins in the cytoplam. D) Hydrophobic hormones easily enter the plasma membrane. Therefore, there is no need for hydrophinic hormone receptors to be on the extracellular surface.arrow_forwardThe hormones known as "catecholamines" (adrenaline, noradrenaline, and dopamine) are not lipid-soluble. Therefore their receptor sites are: O a) On the inside of the plasma membrane O b) On the outside of the plasma membrane O c) In the cell cytoplasm O d) In the cell nucleusarrow_forward
- Recently, a Gα q-coupled receptor was discovered that mediates at least some of the many activities of estrogen. At the time, this discovery generated considerable controversy, as it ran counter to what was then the understanding of how steroid hormone signaling worked. Which of the following observations might have led the investigators to suspect the existence of this newly discovered receptor? A. Activities of estrogen apparent less than 1 minute after application of the hormone B. The growth promoting activity of estrogen C. The presence of estrogen nuclear receptors in cells not previously known to respond to the hormone D. Estrogen is found in much higher concentrations in adult women than adult men E. Uptake of estrogen by target cellsarrow_forwardUnder in vivo conditions, chronic treatment with a noncompetitive antagonist may lead to the up-regulation of the targeted receptor over time. True False Cytokines are peptides that are generally made in advance by specific types of cells, stored in vesicles, and act as autocrine or paracrine factors. True False Thyroid hormone is stored in an extracellular compartment. True Falsearrow_forwardOverexpression of this receptor in the cells of the adrenal gland causes Cushing's syndrome, a disease caused by the overproduction of cortisol. One strategy that scientists have employed to treat this disease is the use of small molecules that bind to, but do not activate, MC2R. This type of molecule is generically referred to as an antagonist. How can an antagonist bind to the same receptor as ACTH but not activate it? O a. The antagonist can bind covalently while ACTH binds non-covalently O b. The antagonist is only partially complimentary to the binding pocket of MC2R O The antagonist binds to ACTH and blocks it from binding to the receptor properly O d. The antagonist is the exact same structure as ACTH but since it is synthetic it doesn't work One cause of Cushing's syndrome is the inappropriate production of GPCRS in the adrenal gland that are not normally present in those cells. When these receptors are activated they result in the production of cortisol. Which statement about…arrow_forward
- Why do peptide and steroid hormones bind different kinds of receptor, and how does this difference affect the resulting signaling pathways in the target cell?arrow_forwardWhat cellular response (up-regulation or down-regulation) would you predict occurs in response to high doses of a drug that binds to a specific hormone receptor? Will more or less of the drug be required for the same response over time? Explain.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
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Intro to Cell Signaling; Author: Amoeba Sisters;https://www.youtube.com/watch?v=-dbRterutHY;License: Standard youtube license