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Cellular and Molecular Biology > Final: Ch 15 G-Protein Coupled Receptors > Flashcards

Final: Ch 15 G-Protein Coupled Receptors Flashcards

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1
Q

what is a G-protein

A

GTP-binding protein

bind GTP/GDP

active when bound to GTP, inactive when bound to GDP

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2
Q

regulation of G-protein genes

A

transcriptional regulation using TF (binds to promoter)

post-translational regulation/modification

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3
Q

examples of post-transcriptional regulation of G-protein genes

A

alternative splicing

capping

polyadenylation

RNAi

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4
Q

G-proteins are anchored in the cell membrane when…

A

GDP bound –> ligand binds –> GTP binds to alpha subunit

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5
Q

4 things GPCR signal transduction pathways have in common

A

receptor with 7 transmembrane alpha helices

coupled trimeric G-protein switch

membrane-bound effector protein

proteins for feedback regulation and desensitization of the pathway

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6
Q

where are the N and C termini of GPCR

A

N-terminus on extracellular face

C-terminus on cytosolic face

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7
Q

B-adrenergic receptors

A

bind hormones like epi and nor-epi

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8
Q

can different subtypes of GPCR bind the same hormone and have different effects?

A

yes

ex. epinepherine (in heart increases contraction, in smooth muscle relaxes)

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9
Q

what happens in fight or flight

A

adrenal gland releases Epi to bind B-adrenergic GPCR in liver/muscle cells

stimulate glycogen breakdown to glucose

high epi in blood

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10
Q

trimeric G-proteins 3 subunits

A

alpha

beta + gamma (complexed together)

linked to membrane by lipids

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11
Q

in resting state, G-alpha subunit has a bound ___ and is complexed to _____

A

GDP, complexed to G-betagamma

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12
Q

binding of ligand to GPCR changes conformation of the receptor and allows…

A

the receptor to bind to G-alpha subunit –> release GDP

GTP binds G-alpha –> release of receptor and G-betagamma

G-alpha binds effector protein

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13
Q

how to detect GPCR-mediated dissociation of the G protein

A

FRET - fluorescence energy transfer

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14
Q

all effector proteins in GPCR pathway are either…

A

membrane bound ion channels

membrane bound enzymes that catalyze formation of 2nd messengers

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15
Q

which subunit of the G-protein determines its function?

A

G-alpha

ex. G-alpha S activates adenylyl cyclase to increase cAMP

G-alpha i inhibits adenylyl cyclase to decrease cAMP

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16
Q

one of the simplest cellular responses to a signal is the opening of…

A

ion channels

ex. open ligand-gated ion channels for neurotransmitters

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17
Q

many nt receptors are…

A

GPCR whose effector proteins are Na or K channels

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18
Q

mAChR are a type of GPCR found in _____ muscle

A

cardiac muscle

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19
Q

what happens when mAChR are activated

A

G-betagamma opens K+ channel (usually G-alpha)

slow heart rate when K+ channels open

efflux of K+ causes hyperpolarization and slows contraction

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20
Q

cones are for ____, rods are for ____/______

A

color, black/white

found in retina, signals processed by visual cortex

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21
Q

rhodopsin

A

light-sensitive GPCR (opsin) that helps rods sense light

G-protein called Transducin (G-alpha-t)

photon-absorbing pigment called retinal

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22
Q

how does rhodopsin differ from other GPCRs

A

absorption of a photon of light is the signal (by retinal), not binding of ligand

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23
Q

what happens when rhodopsin absorbs a photon of light

A

cis –> trans in retinal form causes conformational change in GPCR opsin

rhodopsin binds G-alpha-t subunit and exchanges GDP for GTP

G-alpha-t removes inhibitory gamma segments from phosphodiesterase (PDE), which turns cGMP –> GMP

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24
Q

activation of rhodopsin by light leads to the closing of ____-gated cation channels

A

cGMP

causes membrane potential to become more inside negative (hyperpolarization-less nt released)

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25
Q

in the dark the membrane potential of a rod cell is…

A

-30mV

this is a state of depolarization so in the dark, the rod cell is constantly secreting nt

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26
Q

why is there a constant state of depolarization of resting rod cells

A

large number of open nonselective ion channels that let Na and Ca in

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27
Q

to close the cation channels, the 2nd messenger _____ is turned into

A

cGMP –> GMP

upon absorbing light, cGMP PDE hydrolyzes cGMP to GMP

cGMP releases from gated channels, closing them

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28
Q

the ____ level of cGMP in the dark keeps cGMP gated cation channels open, in the light…

A

high

decrease in cGMP concentration by PDE causes closing of channels and less nt release

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29
Q

what makes the rhodopsin signal transduction pathway so sensitive?

A

signal amplification of the photon of light

each activated opsin activates 500 G-alpha-t molecules which activate the PDE

30
Q

what GAP proteins inactivate G-alpha-t GTP

A

RGS-9 and G-beta-5

hydrolyze GTP –> GDP so PDE is inactivated again

31
Q

Rhodopsin kinase

A

phosphorylates active rhodopsin

arrestin binds after 3 phosphates and prevents transducin activation (G-alpha-t)

32
Q

how do rod cells adapt to varying levels of ambient light – visual adaptation

A

adjusting trafficking of arrestin and transducin

80% of G-alpha-t and G-betagamma move out of the outer segment and 80% of arrestin moves into outer segment in 10 min of moderate light

prevents PDE activation

33
Q

adenylyl cyclase synthesizes ____ from ____

A

cAMP, ATP

34
Q

cAMP activates a _____

A

kinase

35
Q

glycogen

A

a storage polymer of glucose

broken down in liver/muscle cells in response to the hormone epinerpherine

36
Q

all of the effects of cAMP are mediated through activation of which kinase

A

protein kinase A (cAMP dependent protein kinase)

binding of cAMP opens catalytic active site

37
Q

degradation of glycogen is called

A

glycogenolysis

stepwise removal of glucose residues from one end of the polymer by glycogen phosphorylase

38
Q

in the liver, glycogen stores are broken down to ….

A

glucose, which is released into the blood and transported to tissues like muscle and brain for energy

39
Q

2 ways epinerpherine stimulated activation of adenylyl cyclase –> higher cAMP –> PKA activation enhances conversion of glycogen to glucose

A

inhibit glycogen synthesis enzymes

stimulating glycogen degradation enzymes

40
Q

what does PKA do

A

phosphorylates and inactivates glycogen synthase (GS), the enzyme that synthesizes glycogen

phosphorylates the inhibitor of phosphoprotein phosphatase (IP) to inactivate it (so glycogen phosphorylase kinase can break down glycogen)

41
Q

in adipose cells, what does activation of PKA do

A

phosphorylation of a lipase that hydrolyzes stored triglycerides to FA and glycerol for energy

42
Q

is there signal amplification in the cAMP-PKA pathway?

A

yes

GPC hormone receptors are able to diffuse rapidly in the plasma membrane

a single epinerpherine-GPCR complex activates up to 100 G-alpha s molecules –> adenylyl cyclase and so on

43
Q

activation of PKA also stimulates the expression of…

A

many genes, including CREB

leads to long-term effects

44
Q

CRE

A

cAMP response element

binds the phosphorylated form of the TF CREB

45
Q

all genes regulated by PKA have ____

A

CRE

binds the phosphorylated form of the TF CREB

46
Q

CREB TF

A

CRE-binding protein

found in nucleus

47
Q

genomic response of PKA

A

catalytic subunit of PKA targets CREB in nucleus and phosphorylates it

CREB binds to distal promoter (response element) of target gene and recruits co-regulator

stimulates gene transcription

48
Q

a ligand (hormone) can have a non ______ response, a ______ response, or both

A

genomic, genomic

49
Q

what is A kinase-associated protein

A

an anchoring protein that binds PKA to specific locations so it is activated in only those locations

ex. heart muscle cells have AKAP15 near Ca channels

50
Q

AKAP in the outer nuclear membrane

A

localizes PKA and cAMP PDE to outer nuclear membrane

helps catalytic subunits of PKA enter nucleus

allows for negative feedback regulation

51
Q

3 ways to down-regulate signaling through the GPCR/cAMP/PKA pathway

A

affinity of receptor for ligand is decreased when GDP is replaced by GTP in G-alpha

intrinsic GTPase activity of G-alpha hydrolyzes GTP –> GDP (hydrolysis rate increased when G-alpha binds adenylyl cyclase)

cAMP PDE hydrolyzes cAMP –> AMP to end cellular response

52
Q

most GPCRs are also down-regulated by ______-_________

A

feedback repression

end product blocks early step in pathway

53
Q

B-arrestin

A

assists endocytosis of cell-surface receptors

54
Q

phospholipase C (PLC)

A

enzymes that hydrolyze a phosphoester bond to yield 2nd messengers that raise cytosolic Ca2+ levels and remodel actin

activate protein kinase C

55
Q

protein kinase C (PKC)

A

affect cellular growth and differentiation

56
Q

important 2nd messengers are derived from the membrane lipid, ______________

A

phosphatidylinositol (PI)

PI –> PIP2

57
Q

PLC cleaves PIP2 into…

A

DAG (diacylglycerol) and IP3 (inositol triphosphate)

58
Q

DAG is associated with the ______ while IP3 freely _______ in the cytosol

A

membrane, diffuses

59
Q

GPCR that activate PLC increase cytosolic ____ concentration even when the ions are absent from the extracellular fluid

A

Ca2+ concentration

PLC cleaves PIP2 into IP3, which opens IP3 gated-Ca channel in ER lumen

60
Q

what does DAG activate

A

protein kinase C - moves to cytosolic leaflet

61
Q

activation of PKC has what effects

A

growth and metabolism

phosphorylates TF

ex. in liver cells, PKC regulates glycogen metabolism

62
Q

calmodulin

A

small cytosolic switch protein that mediates many cellular effects of Ca ions

63
Q

glycogen breakdown and synthesis is coordinately regulated by which two second messengers

A

Ca2+ and cAMP

levels are regulated by neural and hormonal stimulation

64
Q

why is nitroglycerin used to treat angina

A

decomposes to nitric oxide (NO), which relaxes smc in the heart

65
Q

what is the allosteric effect (Hb) – positive cooperativity

A

Hb binds oxygen – increased affinity in lungs, less in tissue

more binding increases affinity

creates a more dramatic switch

66
Q

basic epi GPCR pathway

A

epi + GPCR –> GTP G-alpha

activate adenylyl cyclase –> higher cAMP

cAMP activates PKA to stimulate breakdown of glycogen OR phosphorylation of TF in the nucleus (ex. CREB)

67
Q

do G proteins usually have short-term or long-term effects?

A

short-term

modify existing enzymes or ion channels

68
Q

structure of inactive PKA

A

tetramer of 2 regulatory subunits and 2 catalytic subunits

each R subunit binds the active site of a C subunit to inactivate

69
Q

how is inactive PKA turned on

A

2 cAMP binds each R subunit

conformational change causes R subunits to release C subunits

70
Q

glycogen phosphorylase kinase

A

glycogen –> glucose activates glycogen phosphorylase

activated by high [Ca2+], PKA

71
Q

glycogen synthase

A

stimulates glycogen formation

inhibited by PKA, PKC

Cellular and Molecular Biology (34 decks)

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