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Biol 432 > Surface Receptors > Flashcards

Surface Receptors Flashcards

1
Q

Gαs-AC Coupled Signaling

step 1

A

1) Epinephrine binds
β-adrenergic
receptor with Gαs

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2
Q

Gαs-AC Coupled Signaling

step 2

A

2) AC activated to produce cAMP

from ATP

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3
Q

Specific Disease of G Protein

Signalling

A 
Specific Disease of G Protein
Signalling: Cholera toxin
(bacterium Vibrio cholerae) blocks
GTPase activity of alpha subunit
and so cAMP stimulation constant
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4
Q

Gαs-AC Coupled Signaling

step 3

A

3) cAMP binds to inhibitory
subunit of protein kinase A
(PKA) and releases enzyme

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5
Q

Gαs-AC Coupled Signaling

step 4

A

4) PKA phosphorylates

substrates

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6
Q

Gαs-AC Coupled Signaling

step 5

A

5) CREB = cAMP response

element binding protein

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7
Q

__ binds to consensus
___ in basal state, but when
____ is activated
to enhance transcription

A

CREB binds to consensus
CRE in basal state, but when
phosphorylated is activated
to enhance transcription

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8
Q

Cell Surface Receptors

4 main types (and one novel) based on structure/function:

A

1) 7 Transmembrane Domain (7 TMD) – G protein Coupled Receptors
(GPRs) - (adenylyl cyclase (AC) or phospholipase C (PLC))

2) Growth Factor Receptors (tyr kinase domain attached)
3) Cytokine Receptors (tyr kinase separate)
4) Guanylyl Cyclase Receptors (cyclase attached)
5) Novel Cell surface receptors – such as ferroportin

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9
Q

Cell Surface Receptors: 7 Transmembrane Receptor/G Protein

Coupled Receptors

A

7 hydrophobic segments span
the membrane; also called
“serpentine” receptors

Extracellular domain: N terminus;
recognizes and binds to ligand

Cytoplasmic domain: C terminus;
hydrophilic; transduce signal via
G proteins

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10
Q

GPR DISEASE

A

Mutations in G protein receptors important
pathology in endocrine disorders; often need
homozygous mutation to have loss of function
since excess receptors; also could have gain of
function, if mutation causes constitutive activation;
a single point mutation may also alter binding
specificity or receptor desensitization

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11
Q

GTP

A

= guanosine triphosphate

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12
Q

GDP

A 
GDP= guanosine diphosphate + free phosphate
(Pi = inorganic phosphate)
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13
Q

G-proteins

A 
• Heterotrimers, subunits = αβγ
• G-proteins identified by the α-subunit
– αs = stimulation of AC
– αi = inhibition of AC
– αq/11 = stimulation of PLC
• α-subunit has GTPase activity
• β/γ act as a dimer
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14
Q

G protein Signaling General Mechanism

step 1

A

1) Inactive complex
(associated
with receptor in
membrane)

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15
Q

G protein Signaling General Mechanism

step 2

A

2) Ligand binds inducing
conformation change in
receptor

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16
Q

G protein Signaling General Mechanism

step 3

A

3) Receptor-G protein
complex forms and
GDP dissociates from
alpha subunit

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17
Q

G protein Signaling General Mechanism

step 4

A

4) GTP binds (GTP

10x>GDP in cytosol)

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18
Q

G protein Signaling General Mechanism

step 5

A

5) Gα-GTP dissociate
from receptor and
beta/gamma subunits

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19
Q

G protein Signaling General Mechanism

step 6a

A

6a) Gα-GTP act on effectors
(depends on alpha subtype
e.g. PLC, AC)

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20
Q

G protein Signaling General Mechanism

step 6b

A

6b) beta/gamma may

also act on effectors

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21
Q

G protein Signaling General Mechanism

step 7

A

7) Intrinsic GTPase of alpha

converts GTP to GDP

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22
Q

G protein Signaling General Mechanism

step 8

A

8) Subunits reassociate

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23
Q

G protein Signaling General Mechanism Regulated by..

A 
Regulated by:
a) GPR-associated
protein (GAP) helps
inactivate Gα-GTP and
acts as scaffold for
assembly
b) Receptor
desensitization (βadrenergic receptor
kinase and arrestin)
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24
Q

αs
Stimulatory
(esp. AC)
effector

A

adenylyl cyclase
ca channels
k channels

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25
Q

ai Inhibitory effector

A

adenylyl cyclase
ca channels
k channels

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26
Q

aq Stimulates PLC effector

A

PLCb

Other ligands for GPCR using alpha q – Angiotensin II,
Bradykinin, Acetylcholine

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27
Q

Phosphatidylinositol (4,5)-bisphosphate

A

(PtdIns(4,5)P2 or PIP2
) is a minor
phospholipid component of cell membranes. PtdIns(4,5)P2 is enriched at the plasma
membrane where it is an important substrate for a number of important signalling
proteins. Phospholipase C hydrolyzes the phosphodiester link in PtdIns(4,5)P2
forming inositol 1,4,5-triphosphate (InsP3) and diacylglycerol (DAG).

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28
Q

IP3

A

IP3 = inositol
triphosphate
(2nd messenger)

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29
Q

DAG

A

DAG =
diacylglycerol
(2nd messenger)

30
Q

Gq-PLC-coupled Signaling

step 1

A

1) Ligand (e.g. Angiotensin II)

binds receptor with Gαq

31
Q

Gq-PLC-coupled Signaling

step 2a

A 
2a) Phospholipase cleavage: PIP2
to IP3
(2nd messenger) causing
release of calcium (2nd messenger)
to cytoplasm from the ER and also
forms DAG (2nd messenger)
32
Q

Gq-PLC-coupled Signaling

step 2b

A

2b) DAG may come
directly from
phosphatidylcholine
cleavage

33
Q

Gq-PLC-coupled Signaling

step 3a

A

3a) calcium activates protein
kinases, promotes secretion,
causes contraction

34
Q

Gq-PLC-coupled Signaling

step 3b

A

3b) DAG second messenger

activates protein kinase C

35
Q

Gq-PLC-coupled Signaling

step 4

A

4) PKC numerous
substrates, some of which
involve transcription effects
in the nucleus

36
Q

Desensitization of the β-adrenergic receptor in G protein Signalling
step 1

A

1) Activation of receptor and AC

37
Q

Desensitization of the β-adrenergic receptor in G protein Signalling
step 2

A

2) Phosphorylation of receptor by
β-adrenergic receptor kinase
βARK , a GRK (G proteincoupled receptor kinase)

38
Q

Desensitization of the β-adrenergic receptor in G protein Signalling
step 3

A

3) Inactive AC; arrestin
binds when Pylated and
blocks association with
G protein

39
Q

Desensitization of the β-adrenergic receptor in G protein Signalling
step 4

A

4) Phosphatase removes phosphate
from receptor, allows G protein
association and activation of AC

40
Q

Cholera toxin – (also known as choleragen and sometimes
abbreviated to CTX, Ctx or CT) is protein complex secreted
by the bacterium Vibrio cholerae. It causes …..

A

Cholera toxin – (also known as choleragen and sometimes
abbreviated to CTX, Ctx or CT) is protein complex secreted
by the bacterium Vibrio cholerae. It causes ADP-ribosylation
of Gαs = inhibits GTPase activity – AC active longer
– In gut = increase water and salt secretion

41
Q

Pertussis toxin is a protein-based AB5-type exotoxin
produced by the bacterium Bordetella pertussis – it also
causes…..

A

Pertussis toxin is a protein-based AB5-type exotoxin
produced by the bacterium Bordetella pertussis – it also
causes ADP-ribosylation of Gαi & Gαo prevents G protein
binding HR – inactive GDP-bound G protein

42
Q

Genetic disorders in α subunits

– Eg. Pseudohypoparathyroidism type Ia (PHP-Ia)

A

Target cell resistance to PTH, with ↑ [PTH]

43
Q 
In Growth Factor Receptors enzyme tyrosine kinase is part
of receptor (2)
A

In Growth Factor Receptors enzyme tyrosine kinase is part
of receptor

1) adds phosphate to substrates that recruit other proteins
= signaling complexes

2) adds phosphate to proteins that are also kinases
= phosphorylation cascades

44
Q

Growth Factor Receptors - Signaling Complexes

Step 1

A

1) Typically dimers form upon
ligand binding (but not
shown here)

45
Q

Growth Factor Receptors - Signaling Complexes

Step 2

A

2) Autophosphorylation

46
Q

Growth Factor Receptors - Signaling Complexes

Step 3

A 
3) recruitment of accessory
proteins (SH2 domains
recognize phosphorylated
tyrosines; SH3 domains
recognize proline rich
sequences)
47
Q

Growth Factor Receptors - Signaling Complexes

Step 4

A

4) SH3 proteins also have

Tyr phosphorylation

48
Q

Growth Factor Receptors - Signaling Complexes

Step 5

A

5) Very large complexes may form

with complicated signalling

49
Q

SH2

A

– src homology

domain (type 2)

50
Q

SH3

A

SH3 – type 3

51
Q

Phosphorylation Cascades

A

e.g., insulin, IGF-1 and epidermal growth factor

52
Q

GRB2

A

GRB2 – growth factor

receptor bound protein

53
Q

SOS

A

son of sevenless

54
Q

MEK

A

mitogen activated

protein kinase

55
Q

ERK

A

extracellular

signal-regulated kinase

56
Q

PI3K

A

= Phosphoinositide 3-

kinases

57
Q

PDK

A

PIP3- dependent kinases

58
Q

PKB

A

protein kinase B (AKT)

59
Q

PI3K/PKB common signalling
pathway plus ___ here
show also ___(PDK)

A

PI3K/PKB common signalling
pathway plus downstream here
show also phosphodependent
kinases (PDK)

60
Q

MAPK

A

MAPK
pathway activated =
mitogen activated
protein kinase

61
Q

Cytokine Receptors – Tyrosine Kinase Separate

A

include receptors for cytokines but also same structure (so same family)
for: erythropoietin, colony-stimulating factor, prolactin (PRL), and growth
hormone (GH – not to be confused with Growth Factors and GFR)

62
Q

2 GH receptors brought together by ___ to signal the recruitment of ___ which is a tyrosine kinase

A

2 GH receptors brought together by GH to signal the recruitment of JAK2 which is a tyrosine kinase

63
Q

STAT

A

= Signal Transducers and Activators of Transcription

64
Q 
SIE, GAS and ISRE
are \_\_\_ DNA
regulatory elements
involved in \_\_\_ control
of GH targets ie \_\_\_
A 
SIE, GAS and ISRE
are STAT-binding DNA
regulatory elements
involved in txnal control
of GH targets ie IGF-1
65
Q

JAK2

A

JAK2 = Janus kinase

66
Q

Guanylyl Cyclase Receptor: The Fourth of the Main Cell Surface
Receptors

A

Atrial natriuretic peptide
p.418 Role in
hypertension, because
it’s a powerful vasodilator

Kinase-like domain
regulates catalytic domain
of guanylyl cyclase

When ligand binds, conf.
change removes inhibitory
control of cyclase

67
Q 
Mechanisms by
which primary
messengers
stimulate
guanylyl cyclase.

Two major
classes of
guanylyl cyclase
(GC) are known: _____

A

membranebound and

soluble.

68
Q

Soluble Guanylyl Cyclase

Cytokines

A

Cytokines are small secreted proteins which mediate and
regulate immunity, inflammation, and hematopoiesis. They must
be produced de novo in response to an immune stimulus. They generally
act over short distances and short time spans and at very low
concentration.

69
Q 
\_\_\_ and \_\_\_ both activate SOLUBLE
guanylyl cyclase (GC) to produce
\_\_\_\_ from GTP which in turn
activates cGMP-dependent protein kinase
(PKG), promoting \_\_\_\_
A 
eNOS and iNOS both activate SOLUBLE
guanylyl cyclase (GC) to produce
cyclicGMP from GTP which in turn
activates cGMP-dependent protein kinase
(PKG), promoting vasorelaxation
70
Q

Hepcidin is a polypeptide hormone that is a ___ regulator of body ___ levels.
Hepcidin is released from the ___ when __ levels are __ and there is
inflammation. Liver Hepcidin release will be inhibited by the need for __ during
____. To control ___ release from the gut, liver and WBCs hepcidin
binds to ____. Hepcidin binding causes ____ degradation. ____
presentation can be controlled in a hepcidin dependent and independent fashion

A

Hepcidin is a polypeptide hormone that is a negative regulator of body iron levels.
Hepcidin is released from the liver when iron levels are high and there is
inflammation. Liver Hepcidin release will be inhibited by the need for iron during
erythropoiesis. To control iron release from the gut, liver and WBCs hepcidin
binds to ferroportin. Hepcidin binding causes ferroportin degradation. Ferroportin
presentation can be controlled in a hepcidin dependent and independent fashion

Biol 432 (8 decks)

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