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Notes taken during lecture

Course Code
Jean Jiang Nash

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LECTURE Feb. 15/2011
Cell signalling pathways in quite a bit of detail for today
Each pathways unique protein involved, signals involved
Different signals different responses to each
G-proteinlinked receptor
GTPase complex receives signal
Alpha swaps GDP to GTP
No signal alpha bound to GDP off
Receptor activated induces conformational change in alpha subunit, which
causes GDP to dissociate, and GTP binds in its place
GTP binding causes further conformational change
oActivated alpha subunit dissociates from beta and gamma
Both can now regulate activity of target proteins
Target proteins convey signal to other proteins
Prolonged stimulation receptor becomes inactive, even if ligand is bound
Arrestin bound to receptor on cytosolic side
Receptor either endocytosed for degradation or it can be recycled for further use
to its pathway
ocAMP activates PKA indirectly, since PKA exist bound to inhibitory
molecules, and cAMP causes inhibitory molecules to fall off
phosphorylate specific substrate proteins
protein phosphatises dephosphorylate target proteins
can dephosphorylate PKA substrates, endocytosis, phosphorylate GPCR to turn
off pathway
oif a pathway can be activated, it should also be shut off
phosphorylated immediately functions
slow response, in contrast, includes altering transcription patterns, etc.
to promote glucose release
inhibits glycogen synthesis
PKA is a kinase will phosphorylate glycogen synthase to inhibit glycogen
Promotes breakdown of glycogen
oSo cell can release glucose
oAlso involve phosphorylation phosphorylate glycogen phosphorylation
Kinase phosphorylates proteins
GPK phosphorylates glycogen phosphorylase
Name of protein tells you the target****
Taking enzymes in cytosol and phosphorylating them thus fast response
oDephosphorylation can be just as fast
Slow response
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