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Lecture 12

Biol 2021- Lecture 12-2.docx

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York University
BIOL 2021
Patricia Lakin- Thomas

Biochemistry – Lecture 12 Chapter 15- Part 2- Cell Communication -G-protein coupled receptors GPCR  G-protein coupled receptors largest family in cell surface -700 GPCR in humans -half of all drugs -GPCR always a multipass transmembrane protein 7 membrane spanning  “serpentine” -ligand binding site outside G-protein binding site inside -its works through trimeric G-protein -3 subunits  ß, α, γ -alpha subunits binds GDP -beta γ gamma work together -alpha γ gamma are membrane bound -B-bound as a peripheral protein to α and γ -many G-proteins -specific for a particular GPCR and for a target -Guanine Nucleotide Exchange Factor (GEF) – in the GPCR activating protein/factor -active receptor is going to cause a conformational (alpha subunit) of G-protein change to give an active G-protein -and then you exchange the GDP for GTP and then it is activated -Activate receptors activates many G-proteins -amplification -> a small signal can go and activate many other G-proteins -the target that it activates are ion channels or enzymes -end signal (inactivates) – alpha subunit has GTPase activity -hydrolyses GDP- GTP  inactivate -inactivate receptor by phophorylation -arrestin protein binds and prevents activating any other G-proteins -arrestin is also an adaptor protein -alpha, beta, gamma  when they are all inactive  they are all together -alpha dissociates and beta nand gamma are together  these are both active -bind GDP  alpha, beta, gamma come back together  become inactive -targets: -enyzmes produce small intracellular mediators  called second messengers -2 Pathways: 1) cyclic AMP  most common  produced by deactivation of a GPCR -found in all animal cells -prokaryotes -not found in plants -made by adencylylcyclase and destroyed by CAMP phosphodiesterase  the enzyme breaks phosphodiester bonds -G-protein that produces it is called Gs -because it is stimulatory -Gs activates cylase  produces CAMP -inhibitor of process  cholera toxin inhibits GTPase activity of alpha subunit of Gs -instead of dropping, cylic AMP levels remain high -has an effect on intestinal epithelial cells -causes an efflux of Cl – and water out of the gut -results in diahhera to death -CAMP targets: -protein kinase (main target) called protein kinase A -4 subunits  2 are regulartory while 2 are catalytic -takes 4 molecules of CAMP to bind and activate -this releases catalytic subunits that then go and phosphorylate other proteins  such as serine and threonine -phosphorylate serine and threonine on other proteins Effects of PKA Activation -D-rapids Effects – seconds -Glycogen mobilization in muscle -Turn off Effects: -CAMP phophodiesterase destroys CAMP -Protein phosphotases  remove phosphates -slow effects -> happen in hours -changes in gene transcription
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