signal trans 3 part 2 Flashcards

1
Q
A
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2
Q

GPCR has – transmembrane alpha helixes

A

7

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3
Q

tf the N terminal is on ext side and C terminal in on the int. side in GPCR.

A

T

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4
Q

glycosylation ; phosphorylation in GPCR

A

N; C terminal in GPRC

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5
Q

rhodopsin recptor

A

GPCR

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6
Q

Largest subunit in gpcr

A

alpha

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7
Q

phillic to phobic on gpcr

A

alpha; betay on gpcr

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8
Q

Guanine nucleotide-binding site (GDP, GTP) and GTPase activity

A

alpha subunit of GPCR

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9
Q

GPCR portion that interacs with effector protein

A

alpha subunit

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10
Q

BY unit of GPCR

A

cov attach to membrane with some int. with effector protein

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11
Q

after ligand bidns GPCR —- —–,

GDP/GTP exchange causes—– with —– to dissociate

A

conf change

alpha subunit with GTP

(GPCR)

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12
Q

seconary enzyme in GPCR

A

will bing alpha subunit with GTP

and intrinsic GTPase activation cause Hydrolysis of GTP to GDP and release of alpha GDP

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14
Q

major mechanism of desensitization of GPCR

A

Receptor phosphorylation by protein kinases

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15
Q

Protein kinase A (PKA); receptor

GPCR-specific protein kinases (GRKs); receptor

A

+/- ligand GPCR-specific

+ ligand

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16
Q

Extracellular enzymes —– or —- many of the small ligands.

A

Extracellular enzymes metabolize or inactivate many of the small ligands.

GPCR inact

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17
Q
A

Extracellular enzymes metabolize or inactivate many of the small ligands.

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18
Q
A

Receptor phosphorylation by protein kinases

GPCR termination

19
Q

—— —— endocytosis accounts for some desensitization

A

Receptor-mediated endocytosis accounts for some desensitization

GPCR inact.

21
Q

Effect of EToh on GABA bidning site

A

Causes membrane potential to become more negative

Increases GABA’s suppression of neural activity

Increases dopamine release

23
Q

Caffeinated Alcohol Drinks

—– Binds to allosteric binding site on GABA-bound receptor

24
Q

TF in : Caffeinated Alcohol Drinks

EToh bidning to GABA receptor keeps it closed

A

F keeps it open

26
Q

GABA Ligand-Gated Ion Channel

A

Anion-Selective (Inhibitory)

27
Q

Adenosine G-Protein-Coupled Receptor thru caffiene stimulant

A

① Blocks adenosine binding site (antagonist)

28
Q

Normally Adenosine G-Protein-Coupled Receptor

A

Suppresses neural activity; increases blood flow

29
RTK
Ligand binding Dimerization Kinase activation then Autophosphorylation of tyrosine residues (cross-phosphorylation)
30
GF binding to RTK
act of RTK bidning of adaptor pro. then RAS act protein
31
Allows increased neural activity Leads to blood vessel constriction, epinephrine release, and increased level of alertness
Caffiene blocking
32
Individual feels sober when highly intoxicated.
end result of cafffiene alcohol drinks
33
Each subunit is a single polypeptide chain consisting of: Large extracellular N-terminal domain for binding ligand Single transmembrane domain Intracellular C-terminal domain with catalytic domains
Enzyme-Linked Receptor
34
dimer; tetramer
RTK; SER threonine kinase
35
effect of MAP Kinase – Effector Protein
36
Receptor Serine/Threonine Kinase Ligand binding to type -- Dimerization with type -- Kinase activation and cross-phosphorylation (Ser/Thr residues) of type ---
Ligand binding to type II Dimerization with type I Kinase activation and cross-phosphorylation (Ser/Thr residues) of type I
39
RAS GDP
attaches to membrane and is converted to active RAS (GTP) upon act of RTK by GF RAS act protein phos it.
40
(serine/threonine kinase
MAP Kinase Kinase Kinase MAP Kinase – Effector Protein
41
clustering adaptin binding clathrin binding
adaptin binding clathrin binding clustering
42
MAP Kinase Kinase Kinase
act by RASGTP
43
threonine/tyrosine kinase)
MAP Kinase Kinase
46
upon act of receptor Serine/Threonine Kinase
SMAD binding and phosphorylation SMAD unfolding and act
47
after act of SMAD
dissociation and dimerization with diff SMAD subtypes translocate to nucleus to alter gene expression
48
binding of act SMAD to another SMAD
Exposure of nuclear localization signal (NLS)
49
Termination of Enzyme linked receptor
Receptor-Mediated Endocytosis (Down-Regulation)