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U-M BIOLCHEM 415 - Cholera and Whooping Cough

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BIOLCHEM 415 1st Edition Lecture 11Outline of Last Lecture I. Biological membranes and their compositionII. Lipids physical propertiesIII. Transport ProteinsIV. Channels and pumpsOutline of Current Lecture V. 7TM Signaling PathwaysVI. Receptor messengers amplify signalsVII. Second messengers amplify signalsVIII. Interference can lead to diseaseCurrent LectureThree basic signal transduction pathways- 7TM receptors- 7 membrane spanning regions- ligand site near extracellular surface- diverse array of signals- second messengers bring intracellular news- amplify signals- cross talk : input from or effect on multiple cellular pathways- ligand binding = conformational change in receptor and activation of heterotrimeric G protein- G proteins have α, β, and γ subunits- signaling triggers amplification1) ligand-receptor complex activates G proteinThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.2) single adenylate cyclase catalyzes synthesis of many cAMP3) cyclic AMP activates protein kinase A which can phosphorylate many target proteinsSignal termination- dissociation of the ligand- decrease levels of hormone in the circulation lead dissociation from receptor- spontaneous hydrolysis of GTP by GTPase activity of Gα- forms inactive heterotrimer and releases target enzymePhosphoinositide cascade- G proteins activate phospholipase C to generate two messengers- regulated by DAG and IP3- DAG brings protein kinase C to plasma membrane- IP3 releases Ca2+ from intracellular storesCa2+ as second messenger- present at low steady state levels in all cells- can bind to protein calmodulin and complex can act as diffusible allosteric effector - Ca2+ overload can cause cell deathMolecular imaging allows you to visual signalingInsulin Receptor- exists as dimer- α and β subunits linked by disulfide bonds- phosphorylated sites become docking sites for insulin-receptor substrates initiating downstream reactionsInsulin signaling termination- dissociation of ligand- reversal of phosphorylations by hydrolysisClinical Insights- defects in pathways = disease- 50% of therapeutic drugs target 7TM receptors- protein kinase inhibitors can be effective anti-cancer drugsCholera toxin targets trimeric G proteins- continuous activation of adenylate cyclase and kinease A- Gαs in permanent ON state- dysregulation of ion movements = dehydration = deathWhooping cough/ pertussis toxin - Gαi remains in permanent OFF state- increased levels of cAMP and phosphorylationsRas frequently mutated in human tumors- leave in permanent ON


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