Fiehn BIS103 lecture 09_fall 2010

Glycogen breakdownsynthesis flux control by

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Glycogen breakdown/synthesis: flux control by allosteric regulation activation AMP inactivation G6P, ATP activation G6P, ATP inactivation AMP
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7 Glycogen breakdown/synthesis: flux control by phosphorylation/signaling cascade barb2right hormonal network cAMP protein kinase A + P* adenylate cylase phosphodiesterase Ca 2+ calmodulin Phosph.phosphatase – P* glucagon epinephrine insulin Phosph.kinase + P* nerve impulse 6 other kinases Glycogen metabolism: regulation by de/phosphorylation
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8 Phosphorylase activity control by protein kinases/phosphatases Protein kinase A is activated by cAMP -PP i adenylate cyclase +H 2 O phosphodiesterase Phosphorylase activity control by protein kinases/phosphatases
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9 Phosphorylase kinase activity control by Ca 2+ dependent calmodulin Phosphorylase activity control by protein kinases/phosphatases Calmodulin Ca 2+ Phosphorylase and P.kinase activity control by phosphoprotein phosphatase Phosphorylase activity control by protein kinases/phosphatases Phosphoprotein Phosphatase-1
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10 Phosphoprotein Phosphatase-1 (less active) Phosphorylase and P.kinase activity control by phosphoprotein phosphatase in muscle Phosphorylase activity control by protein kinases/phosphatases Phosphoprotein Phosphatase-1 (more active) cAMP barb2right protein kinase A barb2left epinephrine insulin-stimulated protein kinase barb2left insulin Glycogen metabolism: epinephrine and insulin are antagonists
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11 Glycogen metabolism: epinephrine (‚adrenaline‘) and insulin are antagonists Insulin Glycogen metabolism: diseases van Gierke’s disease glucose McArdle’s and Hers’ disease Andersen’s disease Cori’s disease Pase kinase deficiency Liver GS deficiency Tarui’s disease F6P F2,6bP
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