Campbell Biology Custom Stony Brook 10 Th Edition
10th Edition
ISBN: 9781269870818
Author: Reece Urry Cain Wasserman Minorsky Jackson
Publisher: PEARSON
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Chapter 11.2, Problem 2CC
WHAT IF? → What would the effect be if a cell made defective receptor tyrosine kinase proteins that were unable to dimerize?
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Discuss Signaling by Receptors that Interact with Cytoplasmic Janus Kinases?
. What would happen in each of the following cases? Assume in each case that the protein involved is a soluble protein, not a membrane protein.
You add a signal sequence (for the ER) to the N-terminal end of a normally cytosolic protein.
You change the hydrophobic amino acids in an ER signal sequence into charged amino acids.
You change the hydrophobic amino acids in an ER signal sequence into other hydrophobic amino acids.
4 You move the N-terminal ER signal sequence to the C-terminal end of the protein.
Cell signaling in plant and animal cells is similar in those ways and different in others. Offer one or more hypotheses for these similarities and differences, and cite specific examples.
Chapter 11 Solutions
Campbell Biology Custom Stony Brook 10 Th Edition
Ch. 11.1 - Explain how signaling is involved in ensuring that...Ch. 11.1 - In liver cells, glycogen Phosphorylase acts in...Ch. 11.1 - Prob. 3CCCh. 11.2 - Nerve growth factor (NGF) is a water-soluble...Ch. 11.2 - WHAT IF? What would the effect be if a cell made...Ch. 11.2 - MAKE CONNECTIONS How is ligand binding similar to...Ch. 11.2 - Prob. 4CCCh. 11.3 - What is a protein kinase, and what is its role in...Ch. 11.3 - When a signal transduction pathway involves a...Ch. 11.3 - What is the actual signal that is being transduced...
Ch. 11.3 - WHAT IF? If you exposed a cell to a ligand that...Ch. 11.4 - How can a targct cell's response to a single...Ch. 11.4 - WHAT IF? If two cells have different scaffolding...Ch. 11.4 - Prob. 3CCCh. 11.5 - Give an example of apoptosis during embryonic...Ch. 11.5 - WH AT IF? If apoptosis occurred when it should...Ch. 11 - What determines whether a cell responds to a...Ch. 11 - How are the structures of a GPCR and an RTK...Ch. 11 - What is the difference between a protein kinase...Ch. 11 - What mechanisms in the cell terminale its response...Ch. 11 - What is an explanation for the similarities...Ch. 11 - Binding of a signaling molecule to which type of...Ch. 11 - The activation of receptor tyrosinc kinases is...Ch. 11 - Lipid-soluble signaling molecules, such as...Ch. 11 - Consider this pathway: epinephrine G...Ch. 11 - Apoptosis involves all but which of the following?...Ch. 11 - Which Observation suggestcd to Sutherland the...Ch. 11 - Protein phosphorylation is commonly involved with...Ch. 11 - DRAW IT Draw the following apoptotic pathway,...Ch. 11 - EVOLUTION CONNECTION Identify the evolutlonary...Ch. 11 - Prob. 10TYUCh. 11 - SCIENCE, TECHNOLOGY, AND SOCIETY The aging process...Ch. 11 - WRITE ABOUT A THEME: ORGANIZATION The properties...Ch. 11 - SYNTHESIZE YOUR KNOWLEDGE There are five basic...
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- More than 500 genes have been identified in the human genome that code for protein kinases. What does such identification imply regarding the role of protein kinases in cellular functions? Explain your answer.arrow_forwardGive typing answer with explanation and conclusion Dimerization of transmembrane receptors can facilitate: ALL OF THESE signal transduction NONE OF THESE cross-phosphorylation tyrosine kinase recruitmentarrow_forwarda) Create a diagram which illustrates the typical signalling mechanism of action of kinase- linked receptors and possible routes of communication (autocrine etc.). Should show the specific molecules involved, the mechanisms of signal transduction and indicate the different pathways that are activated. It should include a specific example of a receptor, ligand and signalling pathway for each general class. Include as wide a variety of ligands and modes of action as you can. for a novel pathway. Superfamily Give the superfamily to which the receptor belongs Accession Give the Uniprot accession number Name Give the molecule name Species Give the species Ligand What is the ligand, or class of ligands which bind to this receptor? What are the physiological processes involved? Is this autocrine, paracrine or endocrine or some combination of them? What is the pathology of the receptor? Key physiological process involved Mechanism of What are the downstream actions of the receptor? Which…arrow_forward
- Cell signaling in plant and animal cells is similar in some ways and different in others. Offer one or more hypotheses for these similarities and differences,and cite specific examples.arrow_forwardDiscuss Concepts Describe the possible ways in which a G-proteincoupled receptor pathway could become defective and not trigger any cellular responses.arrow_forwardRTK: What would the following double mutations mean for the status of the signaling pathway, and the phosphorylation of MAPKK (MEK)? 1. Ligand is bound to the receptor; MAPK T120A mutation (T120 is normally phosphorylated by MAPKK) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEK 2) Ligand is not bound to the receptor; MAPKKK T132E mutation (T132 is normally phosphorylated by Ras) a) Pathway ON (final output is achieved) b) Pathway OFF (no final output) c) Phosphorylation of MAPKK MEK d) NO Phosphorylation of MAPKK MEKarrow_forward
- GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEFarrow_forwardWould like a better explanation on Foxp3. Typed what I know for the first questoin In the discussion section the authors wrote “In a previous study, Dombrowski et al. [44], has reported that Treg cells are able to promote myelination and remyelination and its transcriptional factor, Foxp3, is a good indicator of Tregs activity [21, 45].” Where in the cell does Foxp3 act? The FOXP3 protein is found in an immune system gland called the thymus, where regulatory T cells are produced. Foxp3 is a master regulator of transcription in a specific T-cell type, CD4 (+) regulatory T cells (Treg). Foxp3 is a good indicator of Tregs activity. By what word or words in the quote of question 10 do you know that your answer to question 10 is correct?arrow_forward8 80 wh 가 Vt WI V N Messenger GDP 1 BY G protein Receptor Lumen of endoplasmic reticulum Ca Membrane of endoplasmic reticulum 2 " GDP GTP GTP (5b) Phospholipase C PIP 2 3 IP3 DAG (6c) Calmodulin Protein kinase Protein-P © 2011 Pearson Education, Inc. (4a) 6b Protein kinase C ATP + protein Extracellular fluid (5a) Response in cell (contraction, metabolism, transport) ADP protein- p (6a) Response in cell Response in cell (contraction, secretion) Cytosol Which Ga protein activates phospholipase C? Which secondary messenger opens the ligand gated ion channel? What does a kinase do? What does a phosphatase do?arrow_forward
- . which of the following statements about heterotrimetric G proteins and their receptors is incorrect? A: when GTP binds to the alpha subunit of the G protein, the beta-gamma subunit dissociates from the alpha subunit B: G-protein coupled receptors contain nine transmembrane alpha helices C: binding of arrestin causes removal of the receptor from the membrane D: G protein- coupled receptors may be desensitized by serine phosphorylation I had chosen option A and got it wrong. What is the Correct answer and explain how it is. Also, where did i go wrong in choosing option A?arrow_forwardOf the steps listed below, which problem would take you the longest to realize you had a problem in your RTK (ie the highest number of earlier steps could still occur)? O the RTK cannot autophosphorylate O the RTK cannot phosphorylate downstream kinases the RTK cannot integrate into the membrane the extracellular ligand cannot bind to the RTKarrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, has the highest specificity in binding to the target Protein J?arrow_forward
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