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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
ai Inhibitory effector
adenylyl cyclase ca channels k channels
26
aq Stimulates PLC effector
PLCb Other ligands for GPCR using alpha q – Angiotensin II, Bradykinin, Acetylcholine
27
Phosphatidylinositol (4,5)-bisphosphate
(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).
28
IP3
IP3 = inositol triphosphate (2nd messenger)
29
DAG
DAG = diacylglycerol (2nd messenger)
30
Gq-PLC-coupled Signaling | step 1
1) Ligand (e.g. Angiotensin II) | binds receptor with Gαq
31
Gq-PLC-coupled Signaling | step 2a
``` 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
Gq-PLC-coupled Signaling | step 2b
2b) DAG may come directly from phosphatidylcholine cleavage
33
Gq-PLC-coupled Signaling | step 3a
3a) calcium activates protein kinases, promotes secretion, causes contraction
34
Gq-PLC-coupled Signaling | step 3b
3b) DAG second messenger | activates protein kinase C
35
Gq-PLC-coupled Signaling | step 4
4) PKC numerous substrates, some of which involve transcription effects in the nucleus
36
Desensitization of the β-adrenergic receptor in G protein Signalling step 1
1) Activation of receptor and AC
37
Desensitization of the β-adrenergic receptor in G protein Signalling step 2
2) Phosphorylation of receptor by β-adrenergic receptor kinase βARK , a GRK (G proteincoupled receptor kinase)
38
Desensitization of the β-adrenergic receptor in G protein Signalling step 3
3) Inactive AC; arrestin binds when Pylated and blocks association with G protein
39
Desensitization of the β-adrenergic receptor in G protein Signalling step 4
4) Phosphatase removes phosphate from receptor, allows G protein association and activation of AC
40
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 .....
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
Pertussis toxin is a protein-based AB5-type exotoxin produced by the bacterium Bordetella pertussis – it also causes.....
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
Genetic disorders in α subunits | – Eg. Pseudohypoparathyroidism type Ia (PHP-Ia)
Target cell resistance to PTH, with ↑ [PTH]
43
``` In Growth Factor Receptors enzyme tyrosine kinase is part of receptor (2) ```
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
Growth Factor Receptors - Signaling Complexes | Step 1
1) Typically dimers form upon ligand binding (but not shown here)
45
Growth Factor Receptors - Signaling Complexes | Step 2
2) Autophosphorylation
46
Growth Factor Receptors - Signaling Complexes | Step 3
``` 3) recruitment of accessory proteins (SH2 domains recognize phosphorylated tyrosines; SH3 domains recognize proline rich sequences) ```
47
Growth Factor Receptors - Signaling Complexes | Step 4
4) SH3 proteins also have | Tyr phosphorylation
48
Growth Factor Receptors - Signaling Complexes | Step 5
5) Very large complexes may form | with complicated signalling
49
SH2
– src homology | domain (type 2)
50
SH3
SH3 – type 3
51
Phosphorylation Cascades
e.g., insulin, IGF-1 and epidermal growth factor
52
GRB2
GRB2 – growth factor | receptor bound protein
53
SOS
son of sevenless
54
MEK
mitogen activated | protein kinase
55
ERK
extracellular | signal-regulated kinase
56
PI3K
= Phosphoinositide 3- | kinases
57
PDK
PIP3- dependent kinases
58
PKB
protein kinase B (AKT)
59
PI3K/PKB common signalling pathway plus ___ here show also ___(PDK)
PI3K/PKB common signalling pathway plus downstream here show also phosphodependent kinases (PDK)
60
MAPK
MAPK pathway activated = mitogen activated protein kinase
61
Cytokine Receptors – Tyrosine Kinase Separate
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
2 GH receptors brought together by ___ to signal the recruitment of ___ which is a tyrosine kinase
2 GH receptors brought together by GH to signal the recruitment of JAK2 which is a tyrosine kinase
63
STAT
= Signal Transducers and Activators of Transcription
64
``` SIE, GAS and ISRE are ___ DNA regulatory elements involved in ___ control of GH targets ie ___ ```
``` SIE, GAS and ISRE are STAT-binding DNA regulatory elements involved in txnal control of GH targets ie IGF-1 ```
65
JAK2
JAK2 = Janus kinase
66
Guanylyl Cyclase Receptor: The Fourth of the Main Cell Surface Receptors
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
``` Mechanisms by which primary messengers stimulate guanylyl cyclase. ``` Two major classes of guanylyl cyclase (GC) are known: _____
membranebound and | soluble.
68
Soluble Guanylyl Cyclase Cytokines
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
``` ___ and ___ both activate SOLUBLE guanylyl cyclase (GC) to produce ____ from GTP which in turn activates cGMP-dependent protein kinase (PKG), promoting ____ ```
``` 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
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
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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