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

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

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...

See similar textbooks

Similar questions

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?…
Of 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 RTK
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
Which of the following are activated either directly or indirectly by a heterotrimeric G protein subunit (select all that apply)? O IP, receptor O PIP3-dependent protein kinase O Protein Kinase A O Akt O Phospholipase C O Adenylyl cyclase O Phosphoinositide 3-kinase
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.
Describe what cyclin dependent kinase does in the activation of MPF and how this relates to signal transduction.
Pay close attention to the information related to figure 3.14a and the structure of the PKA catalytic site in this figure. In a few well-written sentences, propose the following: A mutation that would result in PKA becoming a dead kinase*. A mutation that would result in PKA becoming a constitutively active** kinase.
Compare the three kinases - PKA, PKC, and CaMKinase II in terms of activation. What is the initial signal that activates them, what components are part of the kinase, and how does the structure modify when activated?
To which type of protein do cyclin – dependent kinases bind to become active?
Working out the order in which the individual components in a signaling pathway act is an essential step in defining the pathway. Imagine that two protein kinases, PK1 and PK2, act sequentially in a kinase cascade. When either kinase is completely inactivated, cells do not respond to the normal extracellular signal. By contrast, cells containing a mutant form of PK1 that is permanently active respond even in the absence of an extracellular signal. Double mutant cells that contain inactivated PK2 and permanently active PK1 respond in the absence of a signal. Draw out the signaling pathway in a wild-type cell. What outcome is predicted for a double mutant cell with an activating mutation in PK2 and an inactivating mutation in PK1? Explain your reasoning
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!
When a trimeric G protein is activated by GPCR? The three subunit of the G protein remain tightly associated with each other; the GDP bound to the a subunit is phosphorylated to form bound GTP; it dissociates into a free B subunit and an ay subunit Options: hydrolyzed, cleaves, phosphorylate, dephosphorylates, folds, glycosates; gtp, gdp, cgmp, atp, adp, camp; cleaves, phosphorylation, dephosphorylation, unfolds, glcosylates, deglycosylate; leucine kinases, glycine kinase, Tyrosine kinases, valine kinase; triimetization, dimerization, monomerization