cell 3 signaling

GPCR, which domains are regulatory, which are activating modules

Reg = E1 E2 E3

Act = C3 C4

more specific non covalent interactions btwn ligand and receptor means what for Kd?

lower Kd

B adrenergic receptor hormone/analogs: names, Kd, what they do

Epinephrine - Kd = 100, activates pathway

Isoproterenol (IP) - Kd = 10, synthetic agonist mimics epi

Alprenolol (AP) - Kd = 7-11, synthetic antagonist “B blocker”

Practolol (PR) - Kd = 845, also B blocker, high Kd means low affinity, wants to bind some epi sites but not all

FRET - ___ spectrum of donor overlaps with ___ spectrum of the acceptor

emission, absorption

CFP absorption and emission

433, 475

YFP absorption and emission

475, 530

Which switch on G alpha needs to be pried open by a GEF to release the GDP?

switch 1

Which switch of active G alpha brings the 2 domains of AC together in order to make cAMP?

switch 2

one GPCR can activate ___ G alphas, one G alpha activating AC can make cAMP = ____ secondary messangers from ligand binding a GPCR ?

100, 100, 10000

ADP ribosylation by cholera, what is the mechanism and what does it do?

Cholera toxin cleaves nicotinamide off NAD, which leaves ADP-ribose, which is added between the carboxy end of an E on G alpha via a covalent ester bond and the 3’ OH of the ribose

This inhibits G alpha from hydrolyzing GTP, same as giving it nonhydrolyzable GTP, means cAMP constantly being made, which in turn causes lots of PKA activity, which phosphorylates and activates CFTR, causing efflux of Na, Cl, H2O (lots of dehydration)

How does the signal activating PKA get terminated? (cAMP presence)

cAMP phosphodiesterase (PDE