Recitation_7-handout-Simona

Recitation_7-handout-Simona - Simona Tescu [email protected]

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Simona Tescu 04/02/2008 [email protected] 7.05 - Section 05 1/5 RECITATION #7 Covers lectures: 18, 19: Protein modules, Hormone action Exam 2 is this Friday, covering lectures 9-19 (Bartel and Yaffe) Review session: Wednesday (4/2/8) at 7pm, in 34-101. Don’t miss it! Important topics: Blood clot formation Requires: Ca 2+ , platelets, serine proteases Clotting factors exist in an inactive form – zymogens Blood clotting is accomplished by a cascade of zymogen activations The clotting phenomenon is activated by proteolysis => chemical amplifier X ----- > Xa Factor Va, Ca 2+ , Phospholipids (Platelets membranes) Prothrombin (II) ------ > Thrombin (IIa) Fibrinogen (I) ------ > Fibrin (Ia) Factor XIIIa Polymers of fibrin make the blood clot Prothrombin domains: GLA - “ γ -carboxyglutamate” domain o Vitamin K is a cofactor in γ -carboxylation of Glu residues o The first10 Glu residues in the amino-terminal region of prothrombin are carboxylated to γ -carboxyglutamate by a vit K-dependent enzyme system o Prothrombin is thus able to bind Ca 2+ much tighter => prothrombin is anchored to phospholipids membranes derived from blood platelets Kringle domains – bind Va and Xa Ser Protease domain (active thrombin) – o released when Xa cleaves prothrombin o will cleave fibrinogen to fibrin Effects of: I. Dicoumarol – vitamin K antagonist o Found in spoiled sweet clover o anticoagulant o Causes a fatal hemorrhagic disease II. Coumadin (warfarin) – vitamin K antagonist => anticoagulant III. EDTA – chelates Ca 2+ => blood will not clot (anticoagulant)
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Simona Tescu 04/02/2008 [email protected] 7.05 - Section 05 2/5 Small G proteins : Ras When Ras-GTP – protein is ON activates other proteins cell proliferation
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