In early studies of adrenergic signaling, it was thought that the epinephrine receptor and adenylate cyclase were one and the same protein. What kind of evidence would prove otherwise?
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- Name three features common to the activation of cytokine receptors and receptor tyrosine kinases. Name one difference with respect to the enzyme activity of these receptors.Identify which of the following statements is a lie? Select one: a.Diacylglycerol (DAG) and inositol triphosphate (IP3) are byproducts of enzymatic cleaving of PIP2 using phospholipase C while PIP2 formed via enzymatic activity of kinases. b.cAMP is an important second messenger because it serves to activate or inactivate proteins within the cells, especially those cells which their metabolic pathways are regulated by cAMP-dependent kinase (A-kinase). c.Second messengers are molecules that act alternative to signaling molecules to bind to the receptors by altering the structure of cellular proteins.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?
- 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.In the case of GPCR (G protein coupled receptor) signaling pathways, which of the following statements is INCORRECT? The gamma subunit of the trimeric G protein has a transmembrane domain whereas the alpha and beta subunits are peripheral proteins If G alpha was locked in a GTP bound state, it would be bound to the effector enzyme rather than to the beta and gamma subunits. In some but not all signaling pathways, when the beta and gamma subunits are separated from alpha - the beta/gamma pair can also stimulate the activation of effectorsContinuous exposure of a Gαs protein coupled receptor to its ligand leads to a phenomenon known as desensitization. Describe several molecular mechanisms for receptor desensitization. How can a receptor be reset to its original sensitized state? What effect would a mutant receptor lacking serine or threonine phosphorylation sites have on a cell?
- 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.List three ways in which a signal is amplified in a Gprotein-coupled receptor signaling pathway.What are the three steps by which receptor tyrosine kinases typically convey an extracellular signal to another intracellular enzyme?
- What are g-coupled protein receptors? Explain the role they play in cell physiology.Activation of certain GPCRs triggers an intracellular signaling mechanism that involves activation of adenlyl cyclase and an increase of cAMP. Which of the following statements best describes the the events that follow such a cAMP increase? a.) The cAMP increase leads to activation of protein kinase C. b.) The cAMP increase leads to activation of the release of the gamma subunit from the GPCR. c.) The cAMP increase leads to activation of protein kinase A.In the B-acrenergic receptor signaling pathway where desensitization occurs, what protein acts as an effector protein? The activity of the effector protein directly affects the activity of which protein in this pathway? How would the presence of a GAP affect the desensitization process? stimulate it inhibit it have no effect What is the actual mechanism by which desensitization occurs? the receptor is ubiquitinated the hormone is phosphorylated the hormone is degraded the receptor is internalized