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Unformatted text preview: Exam 2 Review • cAMP- generated in liver cells after exposure to adrenaline; Causes adrenaline response when added directly to liver cells • Adenylate Cyclase- regulates cAMP (ATP cAMP); is NOT ALWAYS switched on in cells; has two membrane-bound segments o NEM- poisons AC by covalent modification. o Forskolin- Stimulates AC by binding to catalytic domain, producing a larger response than receptor activation. • cAMP Phosphodiesterase- Competes with AC (cAMP AMP); Always switched on in cells. • Caffiene- a competitive inhibitor of adenosine and phosphodiesterase. • Adrenergic Receptor- contains 7 transmembrane domains; G-protein-coupled receptor; can be activated by overexpression due to dimerization. • G Proteins- made up of α, β, and subunits; β inhibits α from binding GTP ϒ ϒ o α subunit is a slow-action GTPase o Cholera Toxin- Blocks the GTPase activity of the α subunit; Blocks G S Protein activity o Pertussis Toxin- Blocks GTP binding; Blocks G i Protein activity o G S Protein- Stimulates AC o G i Protein- Inhibits AC Substrate Specificity of a Protein Kinase is due to: 1.) Amino Acid Specificity (Ser-OH, Thr-OH, Tyr-OH) 2.) Amino Acid sequence surrounding phosphorylation target (1° structure) 3.) Protein Folding (2° and 3° structure) 4.) Spatial locations in cell of both substrate and kinase • Protein Kinase A- Bonds up to 4 cAMP molecules before the two pseudosubstrate domains release the 2 catalytic domains from the 2 regulatory domains. •...
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- Spring '10
- Pertussis, GTP