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Lecture

Ch. 15 - Cell Communication - Part 2 A summary of the chapter and lecture notes on cell communication, part 2. Includes illustrations and graphics from the textbook.

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Department
Biology
Course
BIOL 2021
Professor
Julie Clark
Semester
Winter

Description
BIOL 2021- April 15 2009 CHAPTER 15 – PART 2: CELL COMMUNICATION G PROTEIN COUPLED RECEPTORS (GPCR) - Largest family - On surface - Take signals from the outside and transfer them - 700 GPCR in human genome - ½ of all drugs are targeted to these receptors/pathways - Always a multipass transmembrane protein with a 7 MEMBRANE SPAN (passes through the plasma membrane 7 times) Figure 1 G proteins - GPCR work through trimeric G-protein (3 subunits)  Alpha subunit binds GDP  Beta and gamma subunits form a complex  Alpha and gamma subunits are membrane bound and have fatty acids integral in plasma membrane  There are many G proteins that are specific for GPCR and target Figure 2 Monomeric G protein (1 subunit) - In trimeric proteins, GEF activated the exchange of GDP for GTP on GPCR (activating pathway) - Active receptor cause a conformational change of G protein to give an active G protein - Then GDP is exchanged for GTP (activated) - Many G proteins are activated by active receptors - Amplification-> small signal amplified to cause a big signal - Targets can be on ion channels or enzymes - Signal is ended by alpha GTPase which hydrolyses GTP-> GDP, making it inactive - TO inactivate receptor, receptor gets phosphorylated (receptor kinase)  Then arrestin protein binds which prevents it from activating any more G proteins Αβγ inactive (GDP bound) Separates to: α (active) and βγ (active) Hydrolysis of GTP: GDP-αβγ (inactive- α reconnect with βγ) Targets: enzyme produced small intracellular mediators (second messengers) 2 PATHWAYS - Cyclic AMP (CAMP) produced - Found in all animal cells, prokaryotes but NOT PLANTS - - Made by adenylyl cyclase - Destroyed by CAMP phosphodiesterase (cleaves phosphodiester bonds) - G protein = G5 = stimulatory - Medically important, G5 activates adenylyl cyclase causing CAMP production Cholera toxin (inhibitor): inhibits GTPase (stops from signalling) activity of α subunit of G5  CAMP remains high instead of dropping as it should  Effect in intestinal epithelial cells  CAMP causes efflux of Cl and water goes into gut (causing diarrhea to death) CAMP targets - Main target is protein kinase A (pkA) - pkA has two regulatory subunits and 2 catalytic subunits  needs four CAMP bound to be active  this releases catalytic subunits (active) which phophorylate proteins  serine/threonine specific amino acids are phosporylated by the subunits - pkA activates different targets in specialized cells EFFECTS OF PKA ACTIVATION - can have rapid effects (seconds) i.e. Glycogen metabolism in muscles - to turn off: 1) CAMP PHOSPHODIESTERKINASE: destroys CAMP 2) Prote
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