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Core II > section 2 old Qs > Flashcards

section 2 old Qs Flashcards

1
Q

why is a receptor necessary for efficient signal transduction

A

d

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2
Q

ionotropic receptor vs ion channel

A

ionotropic receptor can be activated by a ligand binding, opening the receptor and allowing specific ions through
ion channnels just allow diffusion of ions down gradient

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3
Q

hydopathy plots

A

identify hydrophobicity of aa residues to see which is hydrophobic and membrane bounde to predict structure
generated by moving a window over residues, determining + values (lipophilc aa, hydrophobic), and - values (hydrophilic) graphe these, + peakes identify transmembrane domains

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4
Q

T/F all membrane associated proteins have N terminus on extracellular side

A

Flase

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5
Q

with certain receptors active, signaling intermediates dock to cytoplasmic face, what facilitates docking PTM? what is the purpose of docking?

A

d

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6
Q

2 ways to turn off receptors

A

Desensitization, sequestration
desensitization - phosphorylation of receptor subunits causes receptors to be unresponsive to further stimulation, Phosphorylation ovvurs via agonist binding which recuriots phosphorylaiton proteins and subsequite beta-arresting binding, can also be cross phosphoyryaltion or targetting by a second messenger like PKA

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7
Q

modifications of PI on the inositol head group

A 
IP3
PI(3,4,5)P2 - PH domains
PI(4)P
PI(4,5)P2
PI(3,4)P2
PLC cleaves inositol head
PI3 kinase
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8
Q

3 ways of activating phospholipase C

experiment to test mechanism

A

binding to the activated alpha sub unit following GPCR activation
binding to tbe Beta subunit following GPCR activation
Tyrosine Kinase activation forms a phosporylated binding site for PLC to dock
experiment: scratchard analysis of bound:free PLC in aprep with tryosine kinase receptor

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9
Q

in T cell anergy, DAG becomes what and what enzyme

A

phosphatidic acid

DGK

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10
Q

two functions of phosphoinositide lipids

A

docking site for PH domains

regulate ion channel activity

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11
Q

3 fates of arachidonic acid

A

Prostaglandins
Leukotrienes
PP5 activator

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12
Q

whats phosphorylation regulate

A

receptor desensitization

Cell structure and motility

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13
Q

advatage and disadvantage of kinase inhibitor to preven the binding of ATP to an enzyme

A

?

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14
Q

feature of tyrosine kinase

A

size of active site cleft - larger in a tyrosine kinase than a ser/thr kinase

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15
Q

structural feature that enables Cam kinase to remain active without calcium calmodulin bound

A 
phosphorylated site (and substrate still bound to catalytic site)
inactive once phoashpate cleaved by phosphorylase while bound to ca calmodulin
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16
Q

steps of JAK-STAT pathway after ligand and before transcription

A 
phosphorylation of JAKS
phosphorylation of receptor subunits
recruitment of STATs
phosphorylaiton of stats
STAT dissociation
STAT dimerization
nuclear translocation of STATs
17
Q

Catalysis by Ser/Thr phosphotases requireswhat metals

corresponding structural feature for Tyr phosphatases

A

zinc and iron for ser/thr

cysteine for tyr

18
Q

events after stimulation of GPCRs by agonists before GPCR internalization

A

d

19
Q

events after stimulation of GPCRs by agonists before g protein independent signaling

A

d

20
Q

heterologous desensitization of GPCRs

A

receptor desensitized by another recepttor and its sginaling molecule cascades; one agonist can phosphorylate multiple types of receptors and the receptor phosphorylated isnt necessarilly what will be internalized like second messenger kinases

21
Q

homologous desensitization of GPCRs

A

receptor desensitizes itself by signal molecule bound to it, receptor internalized is the same one thats phosphorylated like GPK

22
Q

G alpha proteins

A

Gs

Gi

23
Q

G protein effectors

A

adenylyl cyclace

Raf

24
Q

G rpotein regulators

A

GAP

GEF

25
Q

monmeric

A

Ras

Rho

26
Q

regions of G

A

switch I and II domains within G odomain of G protein alpha subunit
swithc on: GPCR acts as GEF on G domain so conformational change allowing release of GDP and binding of GTP to activate alpha subunits
switch off: RGS ?? protein acts as a GAP to interact with switches to stabliize the transition state and allow more effficienct exchange GTP to GDP inactivates alpha subunit

Core II (11 decks)

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