SEELEY'S ANATOMY+PHYSIOLOGY
SEELEY'S ANATOMY+PHYSIOLOGY
12th Edition
ISBN: 9781260172195
Author: VanPutte
Publisher: RENT MCG
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Chapter 17, Problem 4CT
Summary Introduction

To analyze:

The effect of change in the structure of a subunit of G protein that prevents it from binding to GTP.

Introduction:

The eukaryotes have a special type of transmembrane receptors that are present in the plasma membrane. These are signaling molecules that interact with a particular type of proteins called G-proteins based on their binding ability with the nucleotide guanosine triphosphate and guanosine diphosphate, GTP and GDP respectively.

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Suppose 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?
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…
Hormone 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.…

Chapter 17 Solutions

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