S2 highlights Flashcards
CaM K
calmodulin kinase
calmodulin + ca binds to something (calmodulin kinase) and becomes a kinase
removal of regulatory subunit
autophospohyrylates to activate then Ca leaves and calmodulin leaves but is still partially active if still phosphorylated
MAPK
mitogen activated protein kinase lots of steps last step is MAD kinase kinase \+ P to tyr non receptor Tyr KS
PKA
cAMP activates it
PKB
PDK1 activates
also known as Akt
moves from cytosol to membrane for activation then back to cytosol
gets to membrane by finding PI345P3
PKC
PDK1 adds P to first thr
then auphosp of 2 sites catalytically competent but inactive
Ca and DAG and PLs bind to and opens it and now active
move to PM???
PLC
phospholipase C
turns phosphoinositol into DAG and IP3
by cleaving inositol head group
PP1
protein phosphatase 1
PP2A
Protein phosphatase 2A
hetero trimer
catalytic, regulatory, scaffolding
ser/thr phosphotases
PP2B
calcineruin
ser/thr phosphotase
ca dependendent because it has EF hand domain
regulated by calmodulin in opposition
PP5
activated by a lipid
arachidonic acid removes auto inhibitory domain
IP3
releases calcium from ER
IP3 receptor
DAG
activates PKC
ser/thr phosphotases
need zinc and iron
tyr phosphotases
have cysitein at active site
ph domain
docking site for phospholipid heads
ph domain is on the protein
SRC
non receptor Tyr K
intracellular
no ligand
SERCA
into ER
PMCA
Out from cytosol
VDAC
lets Ca into mitochondria matrix
not just Ca
increases IP3 signal on ER
MCU
mito ca uniporter
when cyto high lets Ca in
NCLX
exports to cyto from mito
sodium or lithium exchanged for Ca
TPC1
on lysosomes
IP3R
on ER
IP3 binds
lets Ca out
Ryn R
EC coupling
voltage gated lets out of ER
PiP3
any combo of 3,4,5
3 needed for docking site
45 substrate with PLC and regulates ion channels
agonist
amplifies state so r cant transduce and R can
antagonisti
binds either and prevents transduction
partial agonist
binds either
amplifies state
protects against other molecule so like if agonist is there it goes to r and if antagonist is there it goes to R
why receptors
convergence
divergence
common pathway
transamplification
G proteins
bind GTP (active) GDP (inactive) GEFs and GTPases GPCR is the GEF (heterotrimeric) monomeric
Galpha s
stimulates AC
Galhpa i
inhibits AC
Galpha q11
activase phospholiapce C
PLC
Galpha 12/13
links GPCR to rho
Ras
monomeric G protein most important regulates cell cycle lipid tail and PTMs cancer source other one have Ras domain to gRASp GTP
Ran
mitoo nuclear import exportin
importin stuff
monomeric G protein
Rab
vessicles
monomeric G protein
Rho
actin cyto skeletin
monomeric G protein
Arf
vessiclse
monomeric G protein
GEF
exchanges GDP for GTP
GAP
GTP to GDP
block GAP
too active downstream effects
cant turn off
guanine nucleotide dissocioaition inhibitors
block GAP
regulate heterotrimeric G protein signaling ?
block receptor
eliminate second messengers
block GAP and GEF
destroy ligand
SOC
low Ca response
channel
Extracellular Ca source
long open
CRAC
special SOC
for low ER Ca stores
Stim
ORai
Stim
identifies low Ca because Ca isnt bound to its EF hand domains
Orai
in PM opened when stim comes together during low Ca
Ca signal types
spark
blips
waves
JAK STAT
ligand binds receptor dimerizeds jak associates (different SOCS blocks) jak auto ps to be active adds p to receptor STAT binds p site on receptor JAK ads p to stat stat dissociates and dimerizes translocate to nucleas as TF PIAS can inhibit STAT to DNA binding
Receptor tyrosine kinase
dimerase
autophospohrylation
ligand is a dimer
selectivity for ser/thr vs tyr
tyr is bigger so the catalytic site is bigger
arachidonic acid derivatives
prostaglandins
thromboxanes/leukotrienes
PP5 activation
stop cAMP
phosphodiesterase PDE
breaks down cAMP
why not delete AC
kill the cell
PI45P2
makes DAG or IP3
IP3 effect
release Ca from ER
PIP3 kinase
adds P to C3 for p345P3 for docking site
phosphatidic acid
DAG + DGK
prostaglandins
vasodilation/constriction
immune responses
platelets
leukotrienes
asthma
FA binding proteins
bring into cell nucleas and transfer to PPAR
PPAR
takes FA and acts as TF