Biology 2e
2nd Edition
ISBN: 9781947172517
Author: Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher: OpenStax
expand_more
expand_more
format_list_bulleted
Concept explainers
Videos
Textbook Question
Chapter 9, Problem 13RQ
A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to be stabilized by binding interactions during dimerization after ligand binding. Which hypothesis regarding the effect of this mutation on EGF signaling is most likely to be correct?
- EGF signaling cascades would be active for longer in the cell.
- EGF signaling cascades would be active for a shorter period of time in the cell.
- EGF signaling cascades would not occur.
- EGF signaling would be unaffected.
Expert Solution & Answer
Trending nowThis is a popular solution!
Students have asked these similar questions
List two ways that GPCR signaling transduction can be turned off (go back to inactive state)
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 ?
Which of the following steps amplify the epinephrine signal response in cells: receptor activation of G protein, G protein activation of adenylyl cyclase, cAMP activation of PKA, or PKA phosphorylation of glycogen phosphorylase kinase (GPK)? Which change will have a greater effect on signal amplification: an increase in the number of epinephrine receptors or an increase in the number of Gαs proteins?
Chapter 9 Solutions
Biology 2e
Ch. 9 - Figure 9.8 HER2 is a receptor tyrosine kinase. In...Ch. 9 - Figure 9.10 In certain cancers, the GTPase...Ch. 9 - Figure 9.17 Which of the following statements...Ch. 9 - Figure 9.18 What advantage might biofilm...Ch. 9 - What property prevents the ligands of cell-surface...Ch. 9 - The secretion of hormones by the pituitary gland...Ch. 9 - Why are ion channels necessary to transport ions...Ch. 9 - Endocrine signals are transmitted more slowly than...Ch. 9 - A scientist notices that when she adds a small,...Ch. 9 - Where do DAG and IP3 originate? They are formed by...
Ch. 9 - What property enables the residues of the amino...Ch. 9 - Histamine binds to the H1 G-protein-linked...Ch. 9 - A scientist observes a mutation in the...Ch. 9 - What is the function of a phosphatase? A...Ch. 9 - How does NF-kB induce gene expression? A small,...Ch. 9 - Apoptosis can occur in a cell when the cell is...Ch. 9 - What is the effect of an inhibitor binding an...Ch. 9 - How does PKC’s signaling role change in response...Ch. 9 - A scientist notices that a cancer cell line fails...Ch. 9 - Which type of molecule acts as a signaling...Ch. 9 - Quorum sensing is triggered to begin when...Ch. 9 - A doctor is researching new ways to treat biofilms...Ch. 9 - What is the difference between intracellular...Ch. 9 - How are the effects of paracrine signaling limited...Ch. 9 - What are the differences between internal...Ch. 9 - Cells grown in the laboratory are mixed with a dye...Ch. 9 - Insulin is a hormone that regulates blood sugar by...Ch. 9 - The same second messengers are used in many...Ch. 9 - What would happen if the intracellular domain of a...Ch. 9 - If a cell developed a mutation in its MAP2K1 gene...Ch. 9 - What is a possible result of a mutation in a...Ch. 9 - How does the extracellular matrix control the...Ch. 9 - A scientist notices that a cancer cell line shows...Ch. 9 - What characteristics make yeasts a good model for...Ch. 9 - Why is signaling in multicellular organisms more...Ch. 9 - Pseudomonas infections are very common in hospital...
Additional Science Textbook Solutions
Find more solutions based on key concepts
A team of eight dogs pulls a sled with waxed wood runners on wet snow (mush!). The dogs have average masses of ...
College Physics
Body, Heal Thyself The precision of mitotic cell division is essential for repairing damaged tissues like those...
Biology: Life on Earth with Physiology (11th Edition)
Why do researchers identify the charophytes rather than another group of algae as the closest living relatives ...
Campbell Biology (11th Edition)
Your bore cells, muscle cells, and skin cells look different because a. different kinds of genes are present in...
Campbell Essential Biology (7th Edition)
2. Whether an allele is dominant or recessive depends on
a. how common the allele is, relative to other alleles...
Campbell Biology: Concepts & Connections (8th Edition)
2. List the subdivisions of the thoracic and abdominopelvic cavities.
Human Anatomy & Physiology
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- The epinephrine signaling pathway plays a role in regulating glucose homeostasis in muscle cells. The signaling pathway is activated by the binding of epinephrine to the beta-2 adrenergic receptor. A simplified model of the epinephrine signaling pathway is represented in Figure 1. Epinephrine Plasma Membrane Beta-2 Adrenergic Receptor (GDP (GDP G Protein GTP GTP Adenylyl Cyclase O It breaks down glycogen O it inhibits the glycolysis process it binds to adenylyl cyclase It phosphorylates phosphorylase kinase It is inhibited by Cyclic AMP ATP Cyclic AMP Protein Kinase A -ATP ADP Phosphorylase Kinase -ATP ADP Glycogen Phosphorylase Glycogen Glucose-1-Phosphate Figure 1. A simplified model of the epinephrine signaling pathway in muscle cells Which is true of Protein Kinase A? Glycolysisarrow_forwardCholera toxins, produced by the pathogenic bacteria Vibrio cholerae, disrupt G Protein Coupled Receptor (GPCR) signaling pathways. They interfere with... the ability of the beta subunit of a G protein to bind to the GPCR the ability of the gamma subunit of a G protein to exchange GDP for GTP the ability of the beta subunit of a G protein to bind to an effector protein the ability of the alpha subunit of a G protein to hydrolyze GTP to GDParrow_forwardAberrant signaling through the EGF receptor signal transduction pathway drives many forms of breast cancer, while misregulation of PI3K drives many prostate cancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, and there are several known activating mutations of PI3K. Would a small molecule that targets PI3K be an effective treatment for a breast cancer that is driven by aberrant signaling through the EGF receptor? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.)arrow_forward
- How could we promote rapid or slow signaling for medical purposes? So there are many examples of slow and rapid signaling via coupled receptors. For an example, salivary gland secretion is rapid signaling and cell growth is slow signaling. These pathways could be twisted and used to resolve medical issues in a more natural and less damaging way. Are there any experiments that have or could be done to test out promoting rapid signaling to speed up slow processes such as cell growth in a severe wound? What experiments have or could be done to test out slowing down signaling that is fast like cells responding to their environment negatively (over-active allergies)? Thank you.arrow_forwardPut the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleusarrow_forwardWhich of the following is True about the STAT signaling cascade? O It amplifies signal for TGF-B family of Growth Factors O It amplifies signal for cytokine receptors O It amplifies signal for receptor tyrosine kinases O It amplifies the signal for Notcharrow_forward
- Binding EGF to the EGF receptor causes phosphorylation of tyrosines on the cytoplasmic tail of the receptor. Which of the following best describes the mechanism by which this phosphorylation activates downstream signaling complexes? Select one A. Causes degradation of receptor by proteasome pathway B. Causes EGF receptor to be internalized so it can interact directly with downstream signaling molecules C. Tyrosine phosphorylation alters 3D structure of downstream signaling proteins causing them to change from an inactive to active conformation D. Causes release of EGF from receptor E. Alters the localization of downstream signaling partners in the cytoplasmarrow_forwardThe 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.arrow_forwardRTKs are receptors made of an extracellular ligand binding domain and an intracellular kinase domain (see image). Insulin binds to its RTK Insulin receptor, causing an increase in glucose absorption and storage in liver cells. EGF binds to its own RTK, EGFR and promotes cell growth through the Ras pathway. a) Explain why the same type of tyrosine kinase in two RTKs can lead to very different cellular responses. Give an example of potential cellular outputs for each of these two RTKs.arrow_forward
- Why do we need to identify and determine the function of every single molecule involved in cell signalling? Provide one concrete example of an application of an elucidated cascade of events in cell signalling. (The answer should be no less than 300 words)arrow_forwardYou are studying the role of CAMP in cell signaling. You hypothesize that 2 intracellular signaling proteins, named GO and TIGERS, interact with each other when cells are treated with an extracellular source of CAMP. The two proteins were tagged with CFP or YFP (CFP = cyan fluorescent protein; YFP = yellow fluorescent protein). CFP is excited by 435 nm light and emits lights at 480 nm. YFP is excited by 480 nm light and emits light at 535 nm. 400 500 Wavelength of Emitted Light 400 500 Wavelength of Emitted Light 600 600 Fluorescence 400 400 500 Wavelength of Emitted Light 600 500 Wavelength of Emitted Light 600 Fluorescence Intensity 400 500 Wavelength of Emitted Light 600 Figure Legend. A. Cells expressing GO-CFP irradiate with 435 nm light. B. Cells expressing TIGERS-YFP and irradiated with 435 nm light. C. Cells expressing TIGERS- YFP and irradiated with 480 nm light. D. Cells expressing GO-CFP and TIGERS-YFP and irradiated with 435 nm light. E. Cells expressing GO-CFP and…arrow_forwardThe secondary messenger cyclic AMP (cAMP) is involved in many different signaling pathways, including the G protein-coupled receptor (GPCR) pathway. Which of the following describes an advantage of using cAMP as a secondary messenger in cell signaling? It conserves energy because cAMP can be converted to ATP. It increases signaling specificity because protein kinase A, the direct effector of cAMP, has few substrates. It prolongs the signal because cAMP is chemically stable and persists for a long time after ligand dissociation. It amplifies the signal because one molecule of activated adenylyl cyclase can produce many molecules of cAMP.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- Biology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStax
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Intro to Cell Signaling; Author: Amoeba Sisters;https://www.youtube.com/watch?v=-dbRterutHY;License: Standard youtube license