You are studying three proteins that you think are important Yor progression through the cell cycle. You know that one of them is a phosphatase (P1) and the other two are kinases ( K1 and K2). You add these enzymes in different combinations as shown below, and find that they have different effects on the activity of a cyclin dependent kinase, cdk2p. cdk2p Inactive cdk2p + K1 cdk2p + K2 cdk2p + K1 + K2 Active Inactive Inactive cdk2p + P1 cdk2p + P1 + K2 cdk2p + P1 + K1 cdk2p + P1 + K1 + K2 Inactive Inactive Active Active

You are studying three proteins that you think are important Yor progression through the cell cycle. You know that one of them is a phosphatase (P1) and the other two are kinases ( K1 and K2). You add these enzymes in different combinations as shown below, and find that they have different effects on the activity of a cyclin dependent kinase, cdk2p. cdk2p Inactive cdk2p + K1 cdk2p + K2 cdk2p + K1 + K2 Active Inactive Inactive cdk2p + P1 cdk2p + P1 + K2 cdk2p + P1 + K1 cdk2p + P1 + K1 + K2 Inactive Inactive Active Active

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9
This phosphatase removes an inhibitory phosphotyrosine phosphate from serine protein kinase, mentioned in question 6, which activates kinase. What phosphatase is it? This is what question 6 says....This is the serine protein kinase that when activated in a complex cyclin, controls onset of mitosis and M-phase of the cell cycle. 1. Cyclin A/B 2. Wee 1 3. TOR (Target of Rapmycin) 4. Cdk1 5. none of the these ***I believe the answer is Cdk1 for number 6, but I could be wrong
You have discovered two new inhibitors that inhibit enzymes involved in the pathway shown below. Both inhibitors are newly identified proteins. You know that one of these proteins is a noncompetitive inhibitor of the G1/S-cyclin dependent kinase (G1/S-Cdk). Another protein is a competitive inhibitor of the phosphatase (ie. a regulatory enzyme) that removes phosphates from phosphorylated Rb. mitogen activated mitogen receptor intracellular signaling pathway activated G,-Cdk and G,/S-čdk inactivated Rb protein active Rb protein inactivated transcription regulator active transcription regulator PHOSPHORYLATION OF Rb TRANSCRIPTION TRANSLATION CELL PROLIFERATION 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?…
Rous Sarcoma Virus can cause cancer in infected cells. The tumor causing nature of the virus is linked to it harbouring a gene that codes for a unique receptor tyrasine kinase (RTK). What is it about the tyrosine kinase that accounts for the tumor-causing nature of the virus? O It is unrelated to any human kinase and thus is able to act uncontrollably in causing cell division. O It cantain activate downstream effectors without binding to a SH2 domain. O It lacks the carboxy-terminal regulatory domain that is present in RTKS of non-cancerous cells.
13) A phosphotase removes an inhibitory phosphotyrosine phosphate from the serine protein kinase, in MPF whcih activates the kinase and triggers the initiation of mitosis. true or false
What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
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.
RAS is a signal transducer that acts as a switch for turning on cell division. Drag the descriptions below to their proper places on the figure to show the sequence of events. When growth factor binds to the receptor, the intracellular domain activates RAS by facilitating exchange of GDP for GTP. When no growth factor is bound to the extracellular receptor, RAS is bound to GDP and is inactive. RAS activates the first of three sequential kinase proteins termed the MAP kinase cascade. Cell proliferation proceeds as the machinery for cell division is set in motion. The end result of the MAP kinase cascade is activation of a transcription factor. Receptor 1 Ras GDP 2 4 5 Growth factor Ras GTP
Non-canonical Hedgehog signaling results in actin cytoskeleton rearrangements, leading to cellmovement and changes in cell shape. Describe how changes to the actin cytoskeleton lead to cellmovement and changes in cell shape.You do not need to draw out the signaling pathway again (#1b). Your answer should focus onthe changes to the actin cytoskeleton. Drawings will be helpful!
Fill in the gaps: For M-Cdk to be activated, inhibitory and activating phosphorylate the mitotic CDK, whilst an activating dephosphorylates the mitotic Cdk. O acetyltranferases, kinase O kinases, acetyltransferase O dehydrogenases, acetyltransferase O phosphatases, acetyltransferase O kinases, phosphatase
Stathmin is phosphorylated by cyclin dependent kinases in response to extracellular signals such as growth factors. To further understand the role of phosphorylation in stathmin function, you decide to treat cells with growth factors in the presence or absence of phosphatase and observe microtubule dynamics. Based on the known function of stathmin, and phosphorylation of stathmin, how would you expect phosphatase treatment to affect microtubule dynamics? A. Decreased frequency of catastrophe in the presence of phosphatase, compared to untreated control B. Increased frequency of catastrophe in the presence of phosphatase, compared to untreated control C. Rapid microtubule polymerization in the presence of phosphatase, compared to untreated control D. Catastrophe frequency is the same in phosphatase treated and control cells
Cyclin-dependent kinases are a type of "microchip" protein that require multiple inputs (i.e., structural alterations) to be activated-- and thus are active only under specific conditions (as shown in the diagram below). How does limiting activity to when all conditions have been met help the cell function properly? INPUTS has this phosphate been removed? been added? has this is cyclin present? phosphate