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Core II > Section 2 > Flashcards

Section 2 Flashcards

1
Q

calcium gradients

A

low cytosol

high extracellular and ER

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2
Q

maint chennels for Ca influx

A

IP3R

RyR

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3
Q

main channels for Ca efflux

A

PMCA
NCX
NCKX
SERCA

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4
Q

types of Ca signals

A

Blip/Quark (single channel - not important)
Puff/Spark
Waves

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5
Q

Ca changes during signalling

A

d

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6
Q

3 functions mediated by Ca signaling

A

T-Cells - increased Ca mediats funciton
Muscle contraction
Neurotransmitter release

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7
Q

tools to observe Ca changes

A

Imaging: fluoresecence
chemical indicators: 2 wavelenght and 1 wavelength
flura 2
genetic indicators like GFP

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8
Q

IP3R

A 
on smooth er
lets Ca out into cytosol
activated by IP3 binding and low Ca
most common
result of second messenger cascade
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9
Q

Ryanodine Receptors

A

in excitable cells

opens for excitation contraction coupling so Ca gets out of sarcoplasmic reticulum

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10
Q

SERCA

A

cytosol to ER/SR

2 Ca for 1 ATP

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11
Q

PMCA

A

1 ca out of cell for 1 atp

high affinity slow activity

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12
Q

NCX and NCKX

A

1 Ca out for 3 Na in
1 Ca and 1 K out for 4 Na in
low afinnitiy but fast activity

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13
Q

CRAC

A

open to get more Ca when ER is empty

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14
Q

Puff/Spark

A

Cooperative activity in a microdomain of IP3R or RYR
Puffs- local, diffuse, super small
sparks - small and localized but bigger than puff?

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15
Q

waves

A

global elevations
domino effect
builds in a direction
intra and intercellular

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16
Q

calmodulin

A

finches

Ca plus calmodulin changes shape and binds to proteins to change them

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17
Q

cAMP

A

2nd messenger

ATP + AC = cAMP

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18
Q

cAMP production protein

A

Adenylyl cyclase AC

activated by G protein

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19
Q

cAMP signaling proteins

A

cAMP turns on PKA

to add P to stuff

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20
Q

cAMP degredation proteins

A

phosphodiesterases to AMP

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21
Q

G protein and cAMP interaction

A

G protein turns on AC to make cAMP

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22
Q

Camp and Ca interactions

A

Ca regulates cAMP
calmodulin upregulates cAMP
calcineurin downregulates
cAMP regulates Ca channels = can let more in for contraction

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23
Q

tools for cAMP

A

inhibit PDE
downstream with CREB
upstream depends on pathway

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24
Q

Cellular processes regulated by by G proteins

A

d

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25
Q

subfamilies of G proteins

A

d

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26
Q

effectors of G proteins

A

d

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27
Q

subtypes of Galpha

A

Gs - AC stim
Gi/o - AC inhibit
Gq - phospholipase activation
G12/13 - GPCR to Rho

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28
Q

PTM of G proteins

A

for membrane targeting
prenylation
myristoylation
palmitoylation

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29
Q

regulators of G proteins

A

GTPase off

GEFs on

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30
Q

techniques to study G proteins

A

toxins

inhibitors and probses

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31
Q

pathologies involving G proteins

A 
Cancer
endocrine disease
psychiatric disorders
cholera
hypertension
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32
Q

groups of drugs that target G proteins and GPCRs

A

target: heterotrimeric G proteins and coupled receptors

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33
Q

Mechanisms that regulate GPCRs

A 
removal of ligand
GTPase activity
desensitization
degredation of GEF
Second messenger elimination
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34
Q

major groups of G proteins

A

heterotrimeric - bind to GPCRs

Smal GTP binding proteins (monomeric)

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35
Q

conserved motifs of G proteins

A

N/TKXD - nucleotide base
GXXXXXGSK/T - phosphate binidng (P loop)
DXXG - guanine

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36
Q

activation/inactivation cycle of G protein regulators

A

d

37
Q

G protein effectors

A

high affininty for GTP bound for and bind swithc domain

38
Q

Ras

A

monomeric G protein

cell proliferation and differentiation

39
Q

Rho

A

monomeric G protein

actin cytoskeleton, gene transcription, lipid metabolism

40
Q

Rab

A

monomeric G protein

Vesicle trafficking and transport

41
Q

Arf

A

monomeric G protein

formation of transport vesicle

42
Q

Ran

A

monomeric G protein
chromosome dynamic
nuclear import/export

43
Q

biological activation of monomeric G protein

A

PTM

44
Q

efffectors of monomeric G protein

A

ser/thr kinass and Tyr kinases

45
Q

switch domain

A

d

46
Q

why signal transduction

A

to dynamically respond to changes in environment

47
Q

different types of transductions

A

contact dependent
paracrine - local
endocrine - everywhere
synaptic

48
Q

divergence

A

one ligand haveing many effects depending on cell type

49
Q

convergence

A

multiple ligands acting via same effector pathway

50
Q

why membrane receptor

A

membranes are not permeable to first messengers

51
Q

definition of receptor

A

saturation, reversal, specificity, reconstitiutin

52
Q

study of receptor fucntion

A

binding assay

biological effector assays

53
Q

study of receptor structure

A

isolation from membrane
sequence analysis
hydropathy plot

54
Q

different classes of receptors defined

A

Defined by second messenger - G protien or ionotropic
defined by function - death receptors
defined by activity - tyrosine kinase, notch signaling

55
Q

structural features of receptor classes

A

dimerization - tyrosine kinase
multiple subunits - ionotropic
multiple membrane spanning domains - G proteins
Signaling complex= death receptors

56
Q

receptor states for agonist/antagonist binding

A

Partial agonists and antagonists can bind ot both
Inverse agonists can bind to small r
Agonists can bind to R
Lig-R can transduce when agonist is around
Lig.r cannot transduce with inverse agonist binds to r
Partial agonist
Depends on which state it binds to
To R can transduce
To r cannot transduce
Preference to bind here with active agonist
Partial agonist binds to r
When antagonist is present
Partial agonist binds to R
Antagonist
Binds to either r or R
antagonist plus R can not transduce, no conformational change

57
Q

hydropathy plots

A 
X axis is aa by position
Tells what each aa is/does 
Higher number more hydrophobic
Charged > polar so charged more negative 
Polar and charged are negative 
So above x axis is in the membrane 
Doesnt show which orientatio
58
Q

protein kinases

A

use ATP to add P to protein

Phosphorylases and pyrophosphorylases are different

59
Q

purpose of kinases

A

mediate both TFs and non genomic signaling

60
Q

types of kinases

A

based on aa they add P to

or substrate protein

61
Q

structural features of kinases

A

regulatory and catalytic domains
some regulatory domains are separate polypeptides
catalytic domain binds to ATP, substrate and mediates PO4 transfer
Specificity for Ser/THr vs Tyr basesd on consensus sequence or catalytic cleft

62
Q

PKA

A

cAMP regulated

separate catalytic and regulatory subunits hetero-tetramer

63
Q

PKB

A

Akt
activated by phosphorylation
translocates to membrane and binds to PIP3

64
Q

PKC

A

activated by Ca and diacylglycerol
translocates to membrane
exists in 4 states
regulated by phosphorylation

65
Q

CaM kinase

A

regulated by Ca indirectly

varying active states

66
Q

different tyrosine kinases

A

receptors
non receptors cytoplasmic
janus kinases non receptor TKs

67
Q

regulation of Tyrsoinekinase

A

autophoshorylation RTKs
Phosphorylinaiton and de phosphorylation Src
SOCS/PIAS for JAK STAT

68
Q

JAK-STAT

A

non tyr k
Regulatsion
SOCS - block JAKs
PIAS - block STATS from binding to DNA

69
Q

MAP kinase regulation

A

activation by sequential phosphorylation
P on both Ser/THr and Tyr
Multisite p of RTKs for signal divergence

70
Q

inositol head group phosphorylation site

A

4C and 5C

71
Q

fate of Bis Pohsphate

A

catabolized by PLC

72
Q

PLC

A

signaling intermediate IP3 and DAG
IP3 activateds intracellular calcium channels
DAG activates PKC
DAG gets P in T cell anergy

73
Q

PLC activation

A

direct -phosphorylation

indirect - g proteins

74
Q

another inosital head group P site

A

3C by PI-3 Kinase

75
Q

PI (3,4,5) tris phosphate

A

docking site with PH domains

Facilitates signal transduction

76
Q

PH domains

A

d

77
Q

structure of PI-3 kinase

A

regulatorey and catalytic subunits

78
Q

how many PI-3 kinases

A

differ by substrate T1,2,3

79
Q

T1 PI3 kinase

A

d

80
Q

phosphoinositides

A 
2nd messengers
docking sites
membrane trafficking
ion cahnnel activity
cell structure
81
Q

source of arachidonic acid

A

phospholipids

82
Q

free arachidonic acid

A

becomes prostaglandind, leukotrienes, thromboxanes
phsyical and patholigic functions
signal via receptors

83
Q

are fatty acids present only as part of phospholipids>

A

no some aer unesterified

they exist as part of teh membrane or are bound to proteins

84
Q

free fatty acids and PGs

A

bind to PPARS (steroid hormone receptor family)

transcription factors

85
Q

maine sphingolipid signaling molecules

A

ceramide

shingosine

86
Q

ceramide and sphingosine functinos

A

apoptosis, enzyme regulaiton, cell motilitiy, gene transcription

87
Q

ceramide source

A

de novo from sphingomyelin and sphiganine

88
Q

shingosine source

A

ceramide

89
Q

is shingosine the signalling molecule

A

no, it is converted to shingosine phosphate and secreted
extracellular S1P activates cognate GPCRs
Shingosiene and S1_ translocate to nuclease to be TF factors on histones

Core II (11 decks)

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