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Core II > Section 2 > Flashcards

Section 2 Flashcards

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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
subfamilies of G proteins
d
26
effectors of G proteins
d
27
subtypes of Galpha
Gs - AC stim Gi/o - AC inhibit Gq - phospholipase activation G12/13 - GPCR to Rho
28
PTM of G proteins
for membrane targeting prenylation myristoylation palmitoylation
29
regulators of G proteins
GTPase off | GEFs on
30
techniques to study G proteins
toxins | inhibitors and probses
31
pathologies involving G proteins
``` Cancer endocrine disease psychiatric disorders cholera hypertension ```
32
groups of drugs that target G proteins and GPCRs
target: heterotrimeric G proteins and coupled receptors
33
Mechanisms that regulate GPCRs
``` removal of ligand GTPase activity desensitization degredation of GEF Second messenger elimination ```
34
major groups of G proteins
heterotrimeric - bind to GPCRs | Smal GTP binding proteins (monomeric)
35
conserved motifs of G proteins
N/TKXD - nucleotide base GXXXXXGSK/T - phosphate binidng (P loop) DXXG - guanine
36
activation/inactivation cycle of G protein regulators
d
37
G protein effectors
high affininty for GTP bound for and bind swithc domain
38
Ras
monomeric G protein | cell proliferation and differentiation
39
Rho
monomeric G protein | actin cytoskeleton, gene transcription, lipid metabolism
40
Rab
monomeric G protein | Vesicle trafficking and transport
41
Arf
monomeric G protein | formation of transport vesicle
42
Ran
monomeric G protein chromosome dynamic nuclear import/export
43
biological activation of monomeric G protein
PTM
44
efffectors of monomeric G protein
ser/thr kinass and Tyr kinases
45
switch domain
d
46
why signal transduction
to dynamically respond to changes in environment
47
different types of transductions
contact dependent paracrine - local endocrine - everywhere synaptic
48
divergence
one ligand haveing many effects depending on cell type
49
convergence
multiple ligands acting via same effector pathway
50
why membrane receptor
membranes are not permeable to first messengers
51
definition of receptor
saturation, reversal, specificity, reconstitiutin
52
study of receptor fucntion
binding assay | biological effector assays
53
study of receptor structure
isolation from membrane sequence analysis hydropathy plot
54
different classes of receptors defined
Defined by second messenger - G protien or ionotropic defined by function - death receptors defined by activity - tyrosine kinase, notch signaling
55
structural features of receptor classes
dimerization - tyrosine kinase multiple subunits - ionotropic multiple membrane spanning domains - G proteins Signaling complex= death receptors
56
receptor states for agonist/antagonist binding
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
hydropathy plots
``` 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
protein kinases
use ATP to add P to protein | Phosphorylases and pyrophosphorylases are different
59
purpose of kinases
mediate both TFs and non genomic signaling
60
types of kinases
based on aa they add P to | or substrate protein
61
structural features of kinases
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
PKA
cAMP regulated | separate catalytic and regulatory subunits hetero-tetramer
63
PKB
Akt activated by phosphorylation translocates to membrane and binds to PIP3
64
PKC
activated by Ca and diacylglycerol translocates to membrane exists in 4 states regulated by phosphorylation
65
CaM kinase
regulated by Ca indirectly | varying active states
66
different tyrosine kinases
receptors non receptors cytoplasmic janus kinases non receptor TKs
67
regulation of Tyrsoinekinase
autophoshorylation RTKs Phosphorylinaiton and de phosphorylation Src SOCS/PIAS for JAK STAT
68
JAK-STAT
non tyr k Regulatsion SOCS - block JAKs PIAS - block STATS from binding to DNA
69
MAP kinase regulation
activation by sequential phosphorylation P on both Ser/THr and Tyr Multisite p of RTKs for signal divergence
70
inositol head group phosphorylation site
4C and 5C
71
fate of Bis Pohsphate
catabolized by PLC
72
PLC
signaling intermediate IP3 and DAG IP3 activateds intracellular calcium channels DAG activates PKC DAG gets P in T cell anergy
73
PLC activation
direct -phosphorylation | indirect - g proteins
74
another inosital head group P site
3C by PI-3 Kinase
75
PI (3,4,5) tris phosphate
docking site with PH domains | Facilitates signal transduction
76
PH domains
d
77
structure of PI-3 kinase
regulatorey and catalytic subunits
78
how many PI-3 kinases
differ by substrate T1,2,3
79
T1 PI3 kinase
d
80
phosphoinositides
``` 2nd messengers docking sites membrane trafficking ion cahnnel activity cell structure ```
81
source of arachidonic acid
phospholipids
82
free arachidonic acid
becomes prostaglandind, leukotrienes, thromboxanes phsyical and patholigic functions signal via receptors
83
are fatty acids present only as part of phospholipids>
no some aer unesterified | they exist as part of teh membrane or are bound to proteins
84
free fatty acids and PGs
bind to PPARS (steroid hormone receptor family) | transcription factors
85
maine sphingolipid signaling molecules
ceramide | shingosine
86
ceramide and sphingosine functinos
apoptosis, enzyme regulaiton, cell motilitiy, gene transcription
87
ceramide source
de novo from sphingomyelin and sphiganine
88
shingosine source
ceramide
89
is shingosine the signalling molecule
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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