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47 Cards in this Set

  • Front
  • Back
Properties of GPCRs
7 transmembrane domains
intracellular domain
extracellular domain
primary site of interaction of GPCR with g-protein is
loop 3
GPCRs respond to
a diverse array of extracellular signals
structural properties of G proteins
three subunits: alpha, beta, gamma
alpha subunit of g preotins is bound to
GDP
diverse combinations of alpha, beta, and gamma can cause
diverse effects
gs, gi, gq
5 beta
11 gamma
specificity of g-protein is dictated by
-different G protein families control different signaling cascades
-a given receptor can bind to multiple ligands with diff. affinities
conformational change in the heterodimer g-protein promotes
nucleotide exchange which is activation
GEF
guanine nucleotide exchange factor
RGS
protein that increases rate of GTP hydrolysis to GDP
GAP
protein that increases GTPase activity
effector molecules
become activated by binding of active G protein subunits
-trigger downstream signaling effects
- typically involved in the production of second messengers
heterologous desensitization
PKA and PKC bind GPCR receptors with and without ligands
they can no longer interact with g-protein
homologous desensitization
kinases only phosphorylate only ligand-occupied GPCRs
these recruit and bind Arr
Arr bound receptor is internalized and degraded/phosphorylated
second messenger properties
small, non-protein molecules
rapidly produced or mobilized
readily diffusible
bind efectors
major second messengers
cyclic AMP
cyclic GMP
IP3
Ca2+
DAG
NO.
____converts ATP to cAMP
Adenylate cyclase
AC is activated by:
inhibited by:
GalphaS
Galphai
an example of cAMP is______
EPAC- a GEF for a small G protein
acts on diverse effector molecules
primary target of cAMP is___
cyclic AMP dependent protein kinase (PKA)
Structure of PKA
2 regulatory subunits and 2 catalytic subunits
PKA phosphorylation of GPCRs leads to
heterologous desensitization
PKA phosphorylates
metabolic enzymes: inhibits gluconeogenesis
CFTR: increases transoprt of salt/water across membrane
CREB: TF, now able to activate transcription of genes containing cAMP response elements
GPCR: heterologous desensitization
Cholera Toxin
ADP ribosylation of GalphaS
so GTP cannot be hydrolyzed to GDP and P
physiological results of cholera toxin
PKA phosphorylates and activates CFTR- leads to secretion of salt into intestinal lumen followed by osmosis of water and massive diarhhea and dehydration and can even lead to death
cGMP causes
vasodilation, smooth muscle relaxation
PLC activated by
Galphaq and beta gamma subunits which are released by G alpha i
PLC can also be activated by
TK and small G proteins and other Galpha subunits
function of PLC
cleaves PIP2 to DAG and IP3
with G alphaq speeds up rxn
PKC in response to DAG
binds DAG leading to partial activation and binds Ca2+ leading to full activation
fully active PKC
phosphorylates lots of sustrates involved in numerous pathways
Ca2+ activates
AC, phospholipase A2
Ca2+ inhibits
AC in some cases
Ca2+ also binds
calmodulin which controls the activity of various calmodulin-dependent kinases/phosphatases
high concentration of Ca2+ triggers opening of
ryanodine receptors in sarcoplasmic reticulum- causes muscle contraction
is iNOS controlled by Ca2+
no but NOS is regulated by Ca2+
free Ca2+ is soaked up by
calmodulin and other ca-binding proteins
SERCA
active pump: pumps Ca2+ back into sarcoplasmic/endoplasmic reticulum
-no muscle contraction
iNOS is destabilized and degraded
cross-talk
transduction pathways are not in solation of each other
-the activity of one cascade can affect the activity of another
-this is why drugs have side effects
qualities of apoptosis
programmed
physiological/pathological
tightly regulated
cell shrinkage
membranes intact
no inflammation
energy required
discrete DNA fragmentation
properties of necrosis
accidental
pathological
unregulated
cell swelling
membranes are destroyed
inflammation
energy not required
randomized DNA breakdown
caspases are ______ to be activated
cleaved
IAP
bind/inhibit caspases
Smac/DIABLO
inhibits IAP
anti-apoptotic proteins
Bcl-2
Bcl-XL
pro-apoptotic proteins
multi-domain
-Bax
-Bak
BH3-domain only
-NOXA
-Bid
-Bim
-Bad
activation of multi domain proteins comes from
activation of BH3 only domains