Biology 2e
2nd Edition
ISBN: 9781947172517
Author: Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher: OpenStax
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Textbook Question
Chapter 9, Problem 29CTQ
What would happen if the intracellular domain of a cell-surface receptor was switched with the domain from another receptor?
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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...
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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
- An extracellular signaling molecule binds to cell surface receptor. This cell surface receptor changes shape and activates a trimeric G-protein. What kind of receptor is this? a) Ion-channel coupled receptor b) Receptor Tyrosine Kinase c) G-Protein coupled receptor d) All of the other answers are correct e) Enzyme-coupled receptorarrow_forwardWhat is the main benefit of cell signaling via direct physical contact and cell signaling over short distances (ex: nerve cell signaling)?arrow_forwardDifferent cell types express different types of receptors; even asingle cell may express multiple receptor types. Explain?arrow_forward
- What common features are shared by most cell signaling systems?arrow_forwardIntegrins have many functions, one of which is sensing connections to the extracellular matrix. What is the role of FAK in integrin signaling?arrow_forwardYou have isolated a new species of infectious bacteria. The bacterium releases a toxin that you believe is adversely affecting heterotrimeric Gs (stimulatory)-protein-based signaling. To explore this hypothesis you use an epithelial cell line that is expressing a cyan fluorescent protein (CFP)-labeled α subunit and a yellow fluorescent protein (YFP)-labeled β subunit of a heterotrimeric Gs-protein. CFP emits blue light and has excitation and emission wavelengths of 440 nm and 490 nm, respectively. YFP emits yellow light and has excitation and emission wavelengths of 490 nm and 527 nm, respectively. To test your hypothesis, you perform two experiments. First, you apply a signaling ligand known to activate this Gs protein and track yellow fluorescence. Second, you apply the signaling ligand and the purified bacterial toxin simultaneously and track yellow fluorescence. Which of the following conclusion will you draw based on the above experimental data? The toxin locks the α subunit…arrow_forward
- The SRP receptor functions in the ER membrane. Which answer best describes its translation process and movement to destination for function?arrow_forwardA) Please explain what a G protein coupled receptor is. Please explain how G protein interacts with this receptor. B) Please explain the kind of reactions that follow binding a specific ligand to a G protein coupled receptor. What do these reactions do in the cell? C) How do these reactions work in the cell. What is the function of these reactions in the cell? How do the reactions proceed?arrow_forwardWhich of the following directly phosphorylate tyrosines to start a kinase protein enzymatic cascade? a) Receptor threonine kinase b) Receptor serine kinase c) Receptor tyrosine kinase d) Receptor guanylyl cyclasesarrow_forward
- Signaling by tyrosine kinase receptors is generally associated with all of the following except: OA) receptor dimerization B) growth factor responses C) heterotrimeric G proteins OD) cross phosphorylation E) generating protein binding sites due to phosphorylationarrow_forward3) The “Met" receptor is a membrane receptor protein responsible for initiating signal transduction pathways that cause cells to divide, among other things. After the Met receptor has been stimulated by its specific growth factor, another protein called c- Cbl will bind to the Met receptor. C-Cbl will then attach a chain of small proteins called ubiquitin to the Met receptor. These chains of ubiquitin help the cell recognize that the Met receptor should undergo receptor-mediated endocytosis, which eventually leads to the destruction of the Met receptor. Circle any answer or answers that include mutations that could cause the cell to potentially become a cancer cell. A) a mutation causing there to be too much ubiquitin protein produced. B) a mutation causing c-Cbl to be inactivated. C) a mutation causing ubiquitin to be inactivated. D) a mutation causing there to be too few Met receptors produced. E) a mutation causing the Met receptor to no longer be able to bind to its growth factor.…arrow_forwardWhat is a signal-transduction pathway? Why are mutations in components of signal-transduction pathways often associated with cancer?arrow_forward
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