1) Why is the GPCR referred to as a GEF? What would occur in G protein signalling if the Ga subunit has a mutation resulting in increased GTPase activity?
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- Place the following events in the proper order to describe the production of a second messenger from a G-protein. 1. Dissociation of G alpha from the beta and gamma subunits in the G protein complex 2. Ligand interaction with the G protein-coupled receptor (GPCR) 3. Recruitment of a G protein to the GPCR and replacement of GDP with GTP on the G alpha subunit 4. Conformational change in the G alpha a subunit causing a decreased affinity for the beta and gamma subunits 5. Activation of an effector, such as adenylyl cyclase to make CAMP, by the active G alpha subunit OA. 4, 5, 1, 2, 3 OB. 4, 3, 2, 1, 5 OC-3, 2, 1, 5, 4 OD. 1, 2, 3, 4, 5 OE. 2, 3, 4, 1,5 QUESTION 17 Kinases are essential in the cell because they directly OA. destroy IP3, turning off that signaling pathway. OB. phosphorylate proteins to cause conformational changes that change their activity. OC. directly activate translation. O D bind hydrophobic hormones in the cytoplasm to activate them. O E. bind and release calcium…Signaling activity of G proteins is controlled by GTPase activating proteins (GAPs) and Guanine exchange factors (GEFs). What are the mechanisms by which GAPS and GEFs control G protein functions? GEFS inhibit G protein functions by stimulating GTP hydrolysis; GAPs activate G protein functions by stimulating GDP-GTP exchange. O GAPS inhibit G protein functions by stimulating GTP hydrolysis; GEFs activate G protein functions by stimulating GDP-GTP exchange. GEFS inhibit G protein functions by stimulating GTP hydrolysis; GAPS activate G protein functions by inhibiting GDP-GTP exchange. GAPs stimulate G protein functions by blocking GTP hydrolysis; GEFS inhibit G protein functions by stimulating GTP-GDP exchange. GAPS inhibit G protein functions by stimulating GDP-GTP exchange; GEFS activate G protein functions by stimulating GTP hydrolysisA mutated form of the α subunit of the heterotrimeric G protein has been identified; this form readily exchanges nucleotides even in the absence of an activated receptor. What would be the effect on a signaling pathway containing the mutated α subunit?
- 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 GDPSuppose that a G protein undergoes a mutation that allows the exchange of bound GTP for GDP to occur in the absence of G protein binding to a receptor. How might this mutation affect signaling involving a GPCR? Which subunit of the G protein is most likely affected by the mutation?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.
- TAS2R38 codes for a G-protein coupled receptor which contributes to the tasting of PTC. What does this tell you about PTC as a type of ligand? a It is a protein-based ligand that can cross the CM into the cell b It is a lipid based ligand that can cross the CM into the cell c It is a protein-based ligand that requires a second messenger d It is a lipid-based ligand that requires a second messengerIn 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 effectorsHormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…
- Some strains of bacteria or microorganisms have developed toxins that can modify the activity of the alpha subunit of G proteins which results in disease. For ex. cholera toxin, produced by Vibrio cholerae, causes ADP ribosylation of the stimulatory Gαs subunit of G proteins. This modification abolishes the GTPase of Gαs, and results in an αs subunit that is always in the “on” or active state. It results in continuous stimulation of adenylyl cyclase (AC). The main cells affected by this are the epithelial cell in gastrointestinal tract. Knowing this altered activity of AC, explain why patients affected by this toxin experience severe diarrhea and dehydration that may result in death.What are the three main parts of a signaling pathway? Give a detailed specific example, such as how epinephrine signals for rapid digestion of glycogen in liver cells.27) One of the main differences between receptor tyrosine kinase (RTK) signaling and G-protein coupled receptor (GPCR) signaling is that: GPCR signaling involves enzyme cascades, while RTK signaling does not. Only RTK signaling involves kinase activity. Only GPCR signaling involves a GTPase. GPCR signaling is more likely to have a short-term, reversible effect.