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Core II > S2 highlights > Flashcards

S2 highlights Flashcards

1
Q

CaM K

A

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

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2
Q

MAPK

A 
mitogen activated protein kinase
lots of steps 
last step is MAD kinase kinase 
\+ P to tyr
non receptor Tyr KS
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3
Q

PKA

A

cAMP activates it

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4
Q

PKB

A

PDK1 activates
also known as Akt
moves from cytosol to membrane for activation then back to cytosol
gets to membrane by finding PI345P3

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5
Q

PKC

A

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???

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6
Q

PLC

A

phospholipase C
turns phosphoinositol into DAG and IP3
by cleaving inositol head group

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7
Q

PP1

A

protein phosphatase 1

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8
Q

PP2A

A

Protein phosphatase 2A
hetero trimer
catalytic, regulatory, scaffolding
ser/thr phosphotases

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9
Q

PP2B

A

calcineruin
ser/thr phosphotase
ca dependendent because it has EF hand domain
regulated by calmodulin in opposition

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10
Q

PP5

A

activated by a lipid

arachidonic acid removes auto inhibitory domain

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11
Q

IP3

A

releases calcium from ER

IP3 receptor

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12
Q

DAG

A

activates PKC

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13
Q

ser/thr phosphotases

A

need zinc and iron

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14
Q

tyr phosphotases

A

have cysitein at active site

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15
Q

ph domain

A

docking site for phospholipid heads

ph domain is on the protein

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16
Q

SRC

A

non receptor Tyr K
intracellular
no ligand

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17
Q

SERCA

A

into ER

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18
Q

PMCA

A

Out from cytosol

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19
Q

VDAC

A

lets Ca into mitochondria matrix
not just Ca
increases IP3 signal on ER

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20
Q

MCU

A

mito ca uniporter

when cyto high lets Ca in

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21
Q

NCLX

A

exports to cyto from mito

sodium or lithium exchanged for Ca

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22
Q

TPC1

A

on lysosomes

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23
Q

IP3R

A

on ER
IP3 binds
lets Ca out

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24
Q

Ryn R

A

EC coupling

voltage gated lets out of ER

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25
Q

PiP3

A

any combo of 3,4,5
3 needed for docking site
45 substrate with PLC and regulates ion channels

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26
Q

agonist

A

amplifies state so r cant transduce and R can

27
Q

antagonisti

A

binds either and prevents transduction

28
Q

partial agonist

A

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

29
Q

why receptors

A

convergence
divergence
common pathway
transamplification

30
Q

G proteins

A 
bind GTP (active)
GDP (inactive)
GEFs and GTPases 
GPCR is the GEF (heterotrimeric)
monomeric
31
Q

Galpha s

A

stimulates AC

32
Q

Galhpa i

A

inhibits AC

33
Q

Galpha q11

A

activase phospholiapce C

PLC

34
Q

Galpha 12/13

A

links GPCR to rho

35
Q

Ras

A 
monomeric G protein
most important
regulates cell cycle 
lipid tail and PTMs 
cancer source 
other one have Ras domain to gRASp GTP
36
Q

Ran

A

mitoo nuclear import exportin
importin stuff
monomeric G protein

37
Q

Rab

A

vessicles

monomeric G protein

38
Q

Rho

A

actin cyto skeletin

monomeric G protein

39
Q

Arf

A

vessiclse

monomeric G protein

40
Q

GEF

A

exchanges GDP for GTP

41
Q

GAP

A

GTP to GDP

42
Q

block GAP

A

too active downstream effects

cant turn off

43
Q

guanine nucleotide dissocioaition inhibitors

A

block GAP

44
Q

regulate heterotrimeric G protein signaling ?

A

block receptor
eliminate second messengers
block GAP and GEF
destroy ligand

45
Q

SOC

A

low Ca response
channel
Extracellular Ca source
long open

46
Q

CRAC

A

special SOC
for low ER Ca stores
Stim
ORai

47
Q

Stim

A

identifies low Ca because Ca isnt bound to its EF hand domains

48
Q

Orai

A

in PM opened when stim comes together during low Ca

49
Q

Ca signal types

A

spark
blips
waves

50
Q

JAK STAT

A 
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
51
Q

Receptor tyrosine kinase

A

dimerase
autophospohrylation
ligand is a dimer

52
Q

selectivity for ser/thr vs tyr

A

tyr is bigger so the catalytic site is bigger

53
Q

arachidonic acid derivatives

A

prostaglandins
thromboxanes/leukotrienes
PP5 activation

54
Q

stop cAMP

A

phosphodiesterase PDE

breaks down cAMP

55
Q

why not delete AC

A

kill the cell

56
Q

PI45P2

A

makes DAG or IP3

57
Q

IP3 effect

A

release Ca from ER

58
Q

PIP3 kinase

A

adds P to C3 for p345P3 for docking site

59
Q

phosphatidic acid

A

DAG + DGK

60
Q

prostaglandins

A

vasodilation/constriction
immune responses
platelets

61
Q

leukotrienes

A

asthma

62
Q

FA binding proteins

A

bring into cell nucleas and transfer to PPAR

63
Q

PPAR

A

takes FA and acts as TF

Core II (11 decks)

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