For a cell line with a mutated Ras protein that is always inactive, which of the following conditions will turn on this signaling pathway? O addition of a drug that prevents protein X from activating Ras O addition of a drug that increases the activity of the receptor tyrosine kinase O addition of a drug that prevents protein X from being activated by the receptor tyrosine kinase O addition of a drug that increases the activity of protein Y

For a cell line with a mutated Ras protein that is always inactive, which of the following conditions will turn on this signaling pathway? O addition of a drug that prevents protein X from activating Ras O addition of a drug that increases the activity of the receptor tyrosine kinase O addition of a drug that prevents protein X from being activated by the receptor tyrosine kinase O addition of a drug that increases the activity of protein Y

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter9: Cell Communication

Section: Chapter Questions

Problem 9TYK

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1. EGF interacts with blank to activate the MAP kinase cascade? G protein coupled receptor; receptor Tyrosine kinase; serine/threonine kinase; cdk 2. When a trimetric G protein is activated by gpcf? The three subuni8of 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 as an ay subunit; none
Which of these BEST describes how the signal is transduced from the EGF receptor to the Ras protein? A. Ras is phosphorylated B. Ras is dephosphorylated C. Ras binds to a GTP molecule D. Ras hydrolyzes a GTP molecule
Which of the following are characteristics of “small” monomeric Ras GTPases? A. Membrane bound B. Act as molecular switches between GTP & GDP C. They interact with receptors directly to regulate upstream events D. They are activated upon GTP binding E. None of the above
Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.
You isolated two mutant cells (Cell A and Cell B) which have a problem in the signal transduction pathway. Both cells show activated response to one of RTK mediated signaling without ligand, suggesting the signaling pathway has been constitutively activated by mutations. You introduced mutant Ras that blocks Ras activation step in both cells. When the mutant Ras was expressed in cell A, the signaling pathway was no longer activated. On the other hand, when the mutant Ras was expressed in cell B, the signaling pathway was still active. From these results; Q1) Which protein of the signaling pathway in Cell A might have the mutation? How does that mutation affect the function of that protein? Why do you think so? Q2) Which protein of the signaling pathway in Cell B might have the mutation? How does that mutation affect the function of that protein? Why do you think so?
Binding EGF to the EGF receptor causes phosphorylation of tyrosines on the cytoplasmic tail of the receptor. Which of the following best describes the mechanism by which this phosphorylation activates downstream signaling complexes? Select one A. Causes degradation of receptor by proteasome pathway B. Causes EGF receptor to be internalized so it can interact directly with downstream signaling molecules C. Tyrosine phosphorylation alters 3D structure of downstream signaling proteins causing them to change from an inactive to active conformation D. Causes release of EGF from receptor E. Alters the localization of downstream signaling partners in the cytoplasm
RTK: 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 MEK
Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleus
do you have any clues? GAP protein helps hydrolyze the GTP to GDP in RAS protein. Argenine 789 residue in GAP protein interacts with GTP in RAS protein. However, Arg 789 is mutated to Alanine. which are true or false? ____We expect Ala789 GAP to have no consequence for cell growth or survival signaling. ____Arg789 stabilizes the T-loop of GAP in the outward (active) position, so we expect Ala789 GAP to have no kinase activity. ___Arg789 participates in the GTP hydrolysis reaction carried out by RAS, so we expect RAS to be catalytically inactive when partnered with Ala789 GAP. ____Arg789 binds in the major groove of the DNA double helix, so we expect Ala789 GAP to be inactive as a transcriptional regulator. __Arg789 interacts with RAS switch 1 and switch 2 regions, so we expect the RAS switch to fail with Ala789 GAP. ____The RAS switch would be locked in the OFF position by Ala789 GAP, so we expect no constitutive RAS signaling and hence no risk of this tumor metastasizing. ____The…
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.
A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to be stabilized by binding interactions during dimerization after ligand binding. Which hypothesis regarding the effect of this mutation on EGF signaling is most likely to be correct? EGF signaling cascades would be active for longer in the cell. EGF signaling cascades would be active for a shorter period of time in the cell. EGF signaling cascades would not occur. EGF signaling would be unaffected.
Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP What effect would this have on downstream cellular events?