Second%20Messengers%20

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Second Messengers Protein Kinases

• Lecture 27 BSCI 420/421 Nov 2002
• When you reach the end of your rope,
• tie a knot and hang on -Anon
• Protein kinases
• cAMP and PKA
• IP3. DAG, Ca2, PKC CaM Kinase,Lecture 27

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Protein kinase structure and Evolutionary
Tree (PKA)
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• Protein kinases, e.g. PKA - A ser, thr kinase

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• 2. cAMP and PKA
• cAMP synthesis cAMP increase in a nerve cell
• in response to serotonin

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Activation of PKA by cAMP
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Gene Enzyme Activation by PKA Inactive
-gtActive enzyme
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Reversal of stimulus 1 min When signal molecule
releases, Receptor returns to initial
state, Galpha hydrolyses GTP -gt GDP releases
from enzyme, Adenylate cyclase becomes
inactive, G subunits form trimer again, cAMP
-gtAMP by phosphodiesrease, PKA C subunits bind to
R subunits and becomeinactive, P-Proteins -gt
Protein Pi by protein phosphatase Some
receptors release inhibitory Galphai, Which binds
to AC and inhibits its activity. Eg.
Prostaglandin E1 binds to inhib receptor and
counteracts Epinephrine activity.
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Table 15-1 cAMP mediated responses Thyroid gland
TSH Thyroid hormone secretion Adrenal
cortex ACTH Cortisol secretion Ovary
LH Progesterone secretion Muscle Adrenaline gly
cogen breakdown Bone parathormone Bone
resorption Liver glucagon glycogen
breakdown The same hormone can have the diff
effects in diff cells. Adrenalin (epinephrine)
above, or stim heartbeat rate in heart muscle
cells. How? Same b-adrenergic receptors. Diff.
Enzymes activated in diff cell types. (Beta
blockers-propanolol)
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2. IP3. DAG, Ca2, PKC CaM Kinase The inositol
phospholipid pathway
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Ca2 control
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Calmodulin
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Regulation of CaM-Kinase II