Which of the outcomes could potentially result if a mutation in the gene encoding the Ga subunit eliminates its GTPase activity? Choose three outcomes. Ga would be ineffective as a signal molecule (that is, it could not activate other proteins). The rate of GTP hydrolysis would increase. The concentration of CAMP in the cell would be continuously elevated. The cell would be unresponsive to molecules that act via CAMP. Go would be activated for an extended period. The signaling pathway could be activated for an extended period, possibly resulting in undesirable cell proliferation.

Which of the outcomes could potentially result if a mutation in the gene encoding the Ga subunit eliminates its GTPase activity? Choose three outcomes. Ga would be ineffective as a signal molecule (that is, it could not activate other proteins). The rate of GTP hydrolysis would increase. The concentration of CAMP in the cell would be continuously elevated. The cell would be unresponsive to molecules that act via CAMP. Go would be activated for an extended period. The signaling pathway could be activated for an extended period, possibly resulting in undesirable cell proliferation.

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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Upon activation by a receptor, a G protein exchanges bound GDP for GTP, rather than phosphorylating GDP that is already bound. Similarly, the a subunit-GTP complex has a slow GTPase activity that hydrolyzes bound GTP, rather than exchanging it for GDP. Describe experimental evidence that would be consistent with these conclusions.
RTKs are receptors made of an extracellular ligand binding domain and an intracellular kinase domain (see image). Insulin binds to its RTK Insulin receptor, causing an increase in glucose absorption and storage in liver cells. EGF binds to its own RTK, EGFR and promotes cell growth through the Ras pathway. a) Explain why the same type of tyrosine kinase in two RTKs can lead to very different cellular responses. Give an example of potential cellular outputs for each of these two RTKs.
You are studying a drug that affects a cAMP signalling pathway that is normally initiated when a signalling molecule binds to a G-protein coupled receptor. You determine that the drug prevents the hydrolysis of GTP bound to G-proteins in this pathway. Describe the impact, if any, that this drug would have on the G-protein coupled receptor (GPCR), assuming that the pathway has been activated by the presence of the signalling molecule (first messenger). Include an explanation for your response.
The G protein coupled receptor (GPCR) pathway elicits diverse intracellular responses in different cells. The basic steps of GPCR signaling are outlined in this diagram. Which of the following statements correctly describes the process of GPCR signaling? The GPCR activation is reversible after the signal of the ligand diminishes. The membrane-embedded enzyme uses GTP as a secondary messenger to initiate gene expression. The ligand attaches to both the GPCR and the membrane-embedded enzyme to activate the GPCR pathway. The ligand-bound GPCR sends a GTP molecule to an enzyme in the membrane and switches it into an active state.
GTP is an important high-energy molecule that facilitates the activation of many cellular sig- nal transduction pathways. Certain genetic dysfunctions can inhibit the ability of a cell to synthesize GTP. Which of the following describes the most direct result of GTP synthesis inhibition? A B с D The cell would be able to carry out reception and transduction but would not be able to produce the cellular response in the relevant signal transduction pathway. The G protein-coupled receptor will not be able to bind corresponding ligands, inhibiting the reception components of the relevant signal transduction pathway. The cell will use ATP instead of GTP to activate the G protein on the intracellular region of the G protein-coupled receptor. The cell would not be able to activate G proteins on the intracellular regions of G pro- tein-coupled receptors.
Describe the events required for full activation of protein kinase B. Name two effects of insulin mediated by PKB in muscle cells.
Nerve-growth factor (NGF) binds to a protein tyrosine kinase receptor. The amount of diacylglycerol in the plasma membrane increases in cells expressing this receptor when treated with NGF. Propose a simple signaling pathway and identify the isoform of any participating enzymes. Would you expect the concentrations of any other common second messengers to increase on NGF treatment?
Key features of signal transduction mechanisms are: specificity, amplification, integration and desensitisation. Give an account of how these features apply to G-protein coupled receptor signalling
The epinephrine signaling pathway plays a role in regulating glucose homeostasis in muscle cells. The signaling pathway is activated by the binding of epinephrine to the beta-2 adrenergic receptor. A simplified model of the epinephrine signaling pathway is represented in Figure 1. Epinephrine Plasma Membrane Beta-2 Adrenergic Receptor (GDP (GDP G Protein GTP GTP Adenylyl Cyclase O It breaks down glycogen O it inhibits the glycolysis process it binds to adenylyl cyclase It phosphorylates phosphorylase kinase It is inhibited by Cyclic AMP ATP Cyclic AMP Protein Kinase A -ATP ADP Phosphorylase Kinase -ATP ADP Glycogen Phosphorylase Glycogen Glucose-1-Phosphate Figure 1. A simplified model of the epinephrine signaling pathway in muscle cells Which is true of Protein Kinase A? Glycolysis
Cholera toxins, produced by the pathogenic bacteria Vibrio cholerae, disrupt G Protein Coupled Receptor (GPCR) signaling pathways. They interfere with... the ability of the beta subunit of a G protein to bind to the GPCR the ability of the gamma subunit of a G protein to exchange GDP for GTP the ability of the beta subunit of a G protein to bind to an effector protein the ability of the alpha subunit of a G protein to hydrolyze GTP to GDP
The Luteinizing hormone receptor (LHR) is a GPCR that predominantly couples to Gαs (G alpha s) G proteins in response to binding of the endogenous ligand luteinizing hormone (LH). Briefly describe how activation of this receptor ultimately leads to protein kinase A (PKA) activation.