You have discovered two new inhibitors that inhibit enzymes involved in the pathway shown below. Both inhibitors are newly identified proteins. Youknow that one of these proteins is a noncompetitive inhibitor of the G1/S-cyclin dependent kinase (G1/S-Cdk). Another protein is a competitive inhibitorof the phosphatase (ie. a regulatory enzyme) that removes phosphates from phosphorylated Rb.mitogenactivated mitogen receptorintracellularsignalingpathwayactivated G,-Cdkand G,/S-čdkinactivatedRb proteinactive Rbproteininactivatedtranscriptionregulatoractive transcriptionregulatorPHOSPHORYLATIONOF RbTRANSCRIPTIONTRANSLATIONCELLPROLIFERATION1. What effect would the noncompetitive inhibitor of the G1/S-Cdk complex have on the Rb protein in the pathway shown above? And what effectwould that have on the final outcome for these cells?2. What effect would the competitive inhibitor of the phosphatase that acts on phosphorylated Rb have on the final outcome for these cells?3. Which of the inhibitors would you prescribe to a cancer patient and why?

Rb protein suppresses tumor cell growth, it plays a key role in the G1 checkpoint of the cell cycle…

1. What effect would the noncompetitive inhibitor of the G1/S-Cdk complex have on the Rb protein in the pathway shown above? And what effect would that have on the final outcome for these cells? 2. What effect would the competitive inhibitor of the phosphatase that acts on phosphorylated Rb have on the final outcome for these cells? 3. Which of the inhibitors would you prescribe to a cancer patient and why?

1. What effect would the noncompetitive inhibitor of the G1/S-Cdk complex have on the Rb protein in the pathway shown above? And what effect would that have on the final outcome for these cells? 2. What effect would the competitive inhibitor of the phosphatase that acts on phosphorylated Rb have on the final outcome for these cells? 3. Which of the inhibitors would you prescribe to a cancer patient and why?

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter37: The Endocrine System

Section: Chapter Questions

Problem 1VCQ: Figure 37.5 Heat shock proteins (HSP) are so named because they help refold misfolded proteins. In...

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A drug that inhibits the kinase activity of AKT would MOST likely have which of the following effects? A. Increased GSK-3b activity and increased CyclinD synthesis B. Increased GSK-3b activity and decreased CyclinD synthesis C. Decreased GSK-3b activity and increased CyclinD synthesis D. Decrease GSK-3b activity and decreased CyclinD synthesis
Predict the effects of the following mutations on the ability of a cell to undergo apoptosis:a. Mutation in Bad such that it cannot be phosphorylated by protein kinase B (PKB)b. Overexpression of Bcl-2c. Mutation in Bax such that it cannot form homodimersOne common characteristic of cancer cells is a loss of function in the apoptotic pathway. Which of the mutations listed above might you expect to find in some cancer cells?
Which of the following elements may be in the transduction part of cell signaling? Select one: a. A phosphatase b. A kinase c. cyclin AMP d. ions e. All answers are correct
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You…
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You add…
This inhibatory kinase phosphorylates an inactive M-Cdk. a) M-kinase b) Wee1 c) CAK d) Cdc25
Based on your understanding of the events surrounding cell death, predict the effect(s) of the following on the ability of a cell to undergo apoptosis:a. Functional CED-9; nonfunctional CED-3b. Active Bax and cytochrome c; nonfunctional caspase-9c. Inactive PI-3 kinase; active Bad
Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
Figure 37.5 Heat shock proteins (HSP) are so named because they help refold misfolded proteins. In response to increased temperature (a “heat shock"), heat shock proteins are activated by release from the NR/HSP complex. At the same time, transcription of HSP genes is activated. Why do you think the cell responds to a heat shock by increasing the activity of proteins that help refold misfolded proteins?
If you have a protein kinase that is regulated by both small molecule inhibitors as well as by phosphorylation, and is part of a cooperative enzyme complex that works as part of a larger pathway involving kinase and GTPase proteins please explain where on this protein regulation could occur, how different types of inhibition could control the function of the protein as well as the function of the complex, and how the protein could regulate other proteins. (This question was previously answered but it was answered incompletely mentioning an herbicide developed in the 1950's. Apparently, it was a plagiarized excerpt from an NCBI article. This is a repost for a full and complete answer. Thank you so much for your help! :) )
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