Cholera toxin ct ct is an ab toxin b is a pore that

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Cholera Toxin (CT) CT is an AB toxin. B is a pore that allows toxin entry into cells A is an enzyme that stabilizes the active GTP- bound form of G Active G activates Protein Kinase A (PKA) PKA activates by phosphorylation a Cl - channel and a Na + - H + exchanger The net consequence is massive loss of NaCl and water from the intestine
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Why use G-proteins? Amplification at two steps: Active receptor can activate multiple G- proteins (by causing GTP to replace GDP) Each downstream target (eg adenylate cyclase) can produce many second messengers (eg, cyclic AMP) Cells can regulate how long the switch is turned on – Different RGS molecules in different cells or at different times
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How Does it Work? Why does GTP binding cause disassociation of from the  subunits? How does hydrolysis of GTP occur to re- set the system?
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The structure of the G subunit Contains 7 repeats of ~40aa: WD repeats
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The GTPase domain of G binds to G in the inactive form
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Phosducin regulates light adaptation in retinal rods In rod cells: – Rhodopsin absorbs photons – Activates G-protein called transducin – Transducin activates cGMP phosphodiesterase degradation of cGMP – One photon degradation of over 100,000 cGMP molecules!! – To dampen the sensitivity, phosducin reduces transducin’s activity Binds G and pulls it into the cytoplasm where it is inactive
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Structure of phodsucin
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Phosducin blocks G binding site of G phosducin G Phosducin binding is negatively regulated by phosphorylation of Serine 73
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How Ras gets activated
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