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Biol 4890 > Powerpoint 4 Chapter 14 > Flashcards

Powerpoint 4 Chapter 14 Flashcards

1
Q

epinephrine receptor

A

beta-andrenergic

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2
Q

epinephrine causes

A

energy-store mobilization

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3
Q

insulin causes

A

increased glucose uptake

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4
Q

EGF causes

A

expression of growth-promoting genes

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5
Q

signal transduction steps

A

1) release of primary messenger 2) reception of primary messenger 3) transduction. receptor releases second messengers 4) Activation of effectors 5) termination

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6
Q

effector

A

controls channels or pumps, enzymes, or proteins that control gene expression

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7
Q

common second messengers

A

cAMP, Ca++, inositol, DAG

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8
Q

three receptor types of signalling pathways

A

G-protein coupled, enzyme linked, ligand gated ion channels

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9
Q

enzyme linked receptors have ? or ? activity

A

cytoplasmic tyrosine kinase, guanylyl cyclase

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10
Q

G-protein receptors AKA

A

7-transmembrane helix receptors

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11
Q

7TM receptors only found in ?

A

eukaryotes

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12
Q

first member of the 7TM family discovered

A

Rhodopsin

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13
Q

?% of therapeutic drugs target 7TM receptors

A

50

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14
Q

bind to andrenergic receptors to activate

A

agonists

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15
Q

inhibit actvation

A

antagonists

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16
Q

types of andrenergic receptors

A

alpha 1 and 2, beta 1,2 and 3

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17
Q

consequence of ligand binding to 7TM

A

conformational change converts receptor into a guanine nucleotide exchange factor. activation of G protein trimer (of alpha, beta, and gamma subunits) because the alpha subunit binds guanyl nucleotides causes the alpha subunit to dissociate.

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18
Q

activation of adenylate cyclase by alpha subunit of G-protein causes

A

conversion of ATP into cAMP

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19
Q

beta-andrenergic receptor is a type of ?

A

7TM receptor

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20
Q

epinephrine binding to beta-andrenergic receptor resulting pathway

A

activation, conformatinal change. activation of G-protein and dissociation of alpha subunit. protein interaction with adenylate cyclase activates. enzymatic reaction to form cAMP. activated protein kinase A.

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21
Q

pathway linking activated Protein Kinase A to mobilization of stored CHO

A

PKA activates phosphoryl kinase. phosphoryl kinase activates phosphorylase. phosphorylase initiates synthesis of glucose from glycogen.

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22
Q

four ways of regulating signaling

A

at the receptor (agonist/antagonist, desensitization), the g-protein itself, second messenger, protein kinases

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23
Q

receptors turned of by?

A

dissociation of signal molecule

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24
Q

receptors desensitized by?

A

phosphorylation of cytoplasmic C-terminal and binding of b-arrestin

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25
Q

G-proteins are timers because..

A

they turn off by hydrolyzing GTP to GDP and Pi

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26
Q

cAMP is degraded by

A

soluble phosphodiesterase

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27
Q

ACE inhibitors are important for?

A

lowering blood pressure

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28
Q

ACE stands for

A

angiotensin converting enzyme

29
Q

angiotensin is produced by ACE and causes

A

vasoconstriction by activating a G-protein that activates Phospholipase C

30
Q

signaling via phospholipase C releases these two secondary messengers from cleavage of PIP2

A

IP3, DAG

31
Q

Protein kinase C can be artificially activated by addition of ?

A

phorbol esters that bind to DAG site and a calcium ionophore

32
Q

IP3 causes

A

rapid release of Ca++

33
Q

PKC ordinarily activated by ?

A

DAG

34
Q

fertilization of an egg causes a wave of ? in the cytoplasm. It can be monitored by fluorescence.

A

Ca++

35
Q

common Ca++ binding site

A

EF Hand motif

36
Q

two important Ca++ binding proteins

A

calmodulin and annexins

37
Q

calmodulin activation causes

A

exposing of hydrophobic patches that bind target proteins. ex. activation of CaM kinase

38
Q

CaM kinase function

A

phosphorylates target proteins that regulate metabolism, ion permeability, and neurotransmitter release

39
Q

common signals of enzyme linked receptors

A

insulin, EGF

40
Q

insulin receptor structure

A

dimer of alpha-beta subunits. insulin binding site is between the two alpha subunits outside of cell

41
Q

result of insulin binding to insulin receptor

A

autophosphorylation followed by phosphorylation of target proteins such as insulin receptor substrates

42
Q

the insulin receptor is a ? kinase

A

tyrosine

43
Q

the insulin receptor substrates share (3)

A

pleckstrin domain, SH2 domains, four Tyr phosphorylation sites

44
Q

pleckstrin domain function

A

binds PIP2

45
Q

SH2 domain function

A

binds phosphotyrosine

46
Q

Akt-2, activated by insulin receptor phosphorylation cascade, is a protein kinase that ?

A

stimulates fusion of GLUT4 receptor vesicles to plasma membrane

47
Q

phosphotyrosine of IRS-1 recruits ?

A

cytosolic PI3 kinase

48
Q

? domain of PI3 kinase binds to IRS-1

A

SH2

49
Q

binding of PI3 kinase to IRS-1 allows ?

A

it to interact with its membrane substrate

50
Q

PI3 kinase produces the secondary messenger ?

A

PIP3

51
Q

phosphatases ? and ? convert PIP3 back to PIP2

A

PTEN and SHIP

52
Q

insulin signaling pathway

A

activated receptor. phosphorylated IRS proteins. localized PI3 kinase. production of PIP3. activated PIP3 dependent protein kinase. activated Akt protein kinase. increased glucose transporter on cell surface.

53
Q

? removes activated receptor

A

receptor recycling

54
Q

Akt is dephosphorylated by ?

A

PHLPP

55
Q

EGF binding to its monomeric receptor causes

A

a conformatinal change that leads to dimerization

56
Q

dimerization of EGF receptor activates ?

A

autophosphorylation of tyrosines in the c-terminal tail

57
Q

phosphotyrosine tails of EGF receptor recruit ?

A

adaptor proteins like Grb-2

58
Q

SH3 domain of Grb-2 binds to ?

A

proline-rich portions of the protein SOS

59
Q

SOS

A

guanine nucleotide exchange factor protein that activates a small G protein called Ras

60
Q

Ras initiates ?

A

phosphorylation cascade by activation of Raf

61
Q

oncogene

A

leads to cancerlike characteristics in susceptible cell types

62
Q

c-Src vs v-Src

A

c-Src contains key tyrosine residue near its C-terminal that when phosphorylated binds to upsteam SH2 region. v-Src lacks this and can not be turned off and leads to unregulated cell growth.

63
Q

? mutations are the most common mutations in tumors

A

Ras

64
Q

overexpression of EGF receptor leads to ?

A

dimerization in the absence of EGF

65
Q

? block dimerization of EGF receptor

A

monoclonal antibodies

66
Q

SH2 and SH3 domains of Src work together to inhibit

A

tyrosine kinase activity

67
Q

90% of patients with chronic myelogenous leukemia have a chromosomal defect that ?

A

activates a tyrosine kinase bcr-abl

68
Q

? is an effective treatment for chronic myelogenous leukemia

A

gleevec

Biol 4890 (16 decks)

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