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BMS100 test 1 > Intracellular signalling and the cell membrane > Flashcards

Intracellular signalling and the cell membrane Flashcards

1
Q

intracellular signals

A

receptors in cell membrane detect extracellular signals and modify cell function

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2
Q

transduction

A

intracellular events that transform the extracellular signal into an intracellular signal

thens there’s more signalling… 2nds messengers…

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3
Q

general intracellular singalling model

A
  1. 1st messenger binds receptor on extracellular domain, (has transmembrane and intercellular domain)
  2. activates enzymes
  3. activates 2nd messenger
  4. activate effectors
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4
Q

what activates effectors?

A

I.e. protein kinases, transcription factors

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5
Q

effector

A

2nd messenger binds and activates other protein, that protein activates another… cascade

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6
Q

amplification

A

increase 2nd messenger

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7
Q

signal termination; 3 ways

A

no 1st messenger or receptor

degrade 2nd messengers

negative feedback

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8
Q

3 types of cell membrane receptors

A
  1. ion channel coupled receptors
    –> signal molecule binds channel which allows entry into cell
  2. enzyme coupled protein receptors
    –> 2 domains of receptor are activated by a signal molecules that forms a dimer causing the catalytic domains to become active
    OR
    –> signal molecule binds receptor and the associated enzyme is activated
  3. g-protein coupled receptors
    –>activate G protein receptor through combining the g protein, enzyme and receptor via the signal molecule
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9
Q

GTPase

A

when GTP hydrolysed to GDP

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10
Q

how do you activate a GPCR receptor? what nucleotide binds the receptor?

A

guanine nucleotide

-activate receptors: activate protein that binds to guanine nucleotide
–>activated G protein modifies enzyme activity
–> GTPase: activates when GTP hydrolyzed to GDP then inactivates

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11
Q

structure of GPCR; what is the receptor and the subunits?

A

receptor- integral transmembrane protein (7 pass)
-3 protein subunits; alpha, beta, gamma

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12
Q

what is an unstimulated GPCRs confirmation?

A

alpha bound to GDP and beta gamma bound to alpha

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13
Q

what is an stimulated GPCRs confirmation?

A

alpha releases GDP, replace with GTP and alpha subunit disengage from beta gamma subunits

-alpha hydrolyzes GTP to GDP and becomes inactivated again

beta gamma subunit can also sometimes activate signals

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14
Q

Gs, Gi, Gq

A

Gs- stimulate
Gi- inhibit
Gq- unique

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15
Q

Gs GPCR pathway

A
  1. ligand binds to receptor associated with Gs
  2. Gs release GDP, alpha subunit binds GTP
  3. Gs binds and activated adenylyl cyclase
    –> adenylyl cyclase enzyme converts ATP –> cAMP
  4. cAMP binds protein kinase A (PKA)
    –>binds and releases inhibitors, left active parts work
  5. PKA phosphorylates a multitude of effector proteins (transduction)
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16
Q

what enzyme does Gs GPCR use? and what does it do?

A

adenylyl cyclase

converts ATP into cAMP

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17
Q

what protein kinase is in a Gs GPCR

A

protein kinase A

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18
Q

what is Gs GPCR secondary messenger

A

cAMP

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19
Q

what happens when Gs GPCR has activated signal transduction (at end of pathway)?

A

activate signal transduction by releasing PKA inhibitors; allows Ca2+ to move down [ ] gradient from storage to cytosol

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20
Q

how to make cAMP and how to inactivate it

A

ATP –> cAMP via adenylyl cyclase

inactivate cAMP –> 5’-AMP via cyclic AMP phosphodiesterase

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21
Q

G protein mechanism of action and what is the exception

A

G protein activated –> 2nd messenger increase or decrease –> modulation of effector that responds directly to 2nd messenger (2nd messenger effector) –> 2nd messenger effector modulates activity of other effectors

exception: sometimes beta gamma subunit activates effectors on their own without using a 2nd messenger

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22
Q

Gs GPCR

-subunit
-subunit activity (impact on 2nd messengers)
-biochemical effects
-a few biologic impacts

A

-subunit: alpha

-subunit activity (impact on 2nd messengers): stimulates adenylyl cyclase –> cAMP production

-biochemical effects: cAMP activates PKA –> phosphorylation of effectors

-a few biologic impacts: glycogenolysis, thyroid hormone synthesis

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23
Q

Gi GPCR

-subunit
-subunit activity (impact on 2nd messengers)
-biochemical effects
-a few biologic impacts

A

-subunit: alpha

-subunit activity (impact on 2nd messengers): inhibits adenylyl cyclase –> decreased cAMP production

-biochemical effects: decreased PKA activation

-a few biologic impacts: inhibition of glycogenolysis, thyroid hormone synthesis etc.

-subunit: beta gamma

-subunit activity (impact on 2nd messengers): activates K+ channels (no 2nd messenger involved)

-biochemical effects: more negative cell membrane potential

-a few biologic impacts: reduction of heart rate

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24
Q

Gq GPCR

-subunit
-subunit activity (impact on 2nd messengers)
-biochemical effects
-a few biologic impacts

A

-subunit: alpha

-subunit activity (impact on 2nd messengers): activates phospholipase C –> IP3 and DAG production

-biochemical effects:
-IP3–> calcium release rom ER
-DAG–> activation of PKC

-a few biologic impacts

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25
what is the differences between the GPCRs in terms of which subunits they have?
Gs and Gq only have alpha subunit, Gi has alpha and beta gamma
26
Gq GPCR; what cleaves the secondary messengers?
phosholipase C
27
how do calcium and calmodulin work in a Gq GPCR?
calcium binds calmodulin -resting cell has no calcium in the cytosol, more in ER and extracellular space -[ ] gradient, want to enter cytosol, increase [ ] in cytosol then bind to calmodulin = effect -activate calmodulin with 4 Ca2+ --> bind effectors (ie. calmodulin kinases)
28
what are the steps of a Gq GPCR?
1. ligand bind receptor associated with Gq GPCR 2. Gq alpha activates phospholipase C 3. phospholipase C cleaves a membrane lipid into IP3 and diacyl glycerol -membrane lipid = PIP2 -IP3 is water soluble- enters the cytosol -DAG is lipid soluble- stays within the cell membrane and diffuses 4. IP3 activates Ca2+ release channel in ER (ER --> cytosol) 5. Ca2+ and DAG activates protein kinase c (PKC) 6. PKC (2nd messenger-activated effector) can modulate activity of other effectors... Ca2+ can also bind calmodulin
29
Gi GPCR which subunit has the effect? which channel does it open?
beta gamma subunit opens the K+ channel K+ leaves the cell, makes it more negative
30
example of an ion channel coupled receptor
Na+/K+ ATPase
31
Na+/K+ ATPase
3 Na+ out 2 K+ in -Na+/K+ ATPase and K+ channel cause negative inside with low cytosolic [Na+] and high [K+] --> Na+ wants to diffuse into cell if Na+ channels open to make the membrane potential more + -very low Ca2+ inside the cell, wants to move in
32
depolarization vs hyper polarization
let Na+ enter through channel opening= depolarization (become more positive) depolarization phase, the gated sodium ion channels on the neuron's membrane suddenly open and allow sodium ions (Na+) present outside the membrane to rush into the cell. As the sodium ions quickly enter the cell, the internal charge of the nerve changes from -70 mV to -55 mV. hyperpolarization= K+ channels let K+ leave and inside becomes more negative Hyperpolarization is when the membrane potential becomes more negative at a particular spot on the neuron's membrane, while depolarization is when the membrane potential becomes less negative (more positive). -many receptors can open ion channels after they bind a ligand (1st messenger) -i.e. calcium enters and calmodulin binds
33
enzyme coupled receptors; what are the 2 possibilities for the cytosolic domain?
intrinsic enzyme activity (I,.e receptor tyrosine kinase) or direct association with an enzyme
34
Gq GPCR what are the secondary messengers?
IP3 and DAG
35
what do the Gq GPCR secondary messengers do?
-IP3--> calcium release rom ER -DAG--> activation of PKC
36
Gq GCPR
-uses Ca2+, IP3, DAG as 2nd messengers -IP3 causes release of calcium from storage in ER -calcium binds and activates many proteins/effectors --> calcium binding protein is calmodulin
37
what binds Ca2+ in a Gq GPCR? how many calcium need to bin it?
calmodulin and 4 calcium
38
which membrane lipid gets cleaved into diacylglycerol DAG and IP3 in a Gq GPCR?
PIP2
39
enzyme coupled receptors
transmembrane proteins with ligand-binding domain on outer surface of plasma membrane - usually 1 transmembrane domain
40
what does ligand binding do to a receptor tyrosine kinase?
cause it to dimerize and activates tyrosine kinase within the receptor
41
receptor tyrosine kinase
binding of ligand dimerizes the receptor and activates tyrosine kinase within the receptor -->phosphorylation by the receptor on its own tyrosine residues activates the receptor --> further signaling
42
what type of activity does a receptor tyrosine kinase have?
intrinsic kinase activity: i.e. receptor phosphorylates itself on specific residues of the intracellular face of the receptor
43
what are some ligand examples that can bind a receptor tyrosine kinase?
insulin, cytokines, growth factors
44
steps of receptor tyrosine kinases
1. ligand binds to receptor monomers 2. receptor dimerizes and each 1/2 phosphorylates the tyrosine residue on the other 1/2 3. signalling proteins then bind to the phosphorylated receptor and also become activated --> signal cascade
45
receptor tyrosine kinase signalling options: phospholipase C
same as Gq GPCR IP3 and DAG --> PKC
46
receptor tyrosine kinase signalling options: ras cascade
1. ras (small intracellular G protein) sees activated RTK and activates itself via binding GTP 2. Was activated Raf (small plasma membrane associated G protein) 3.activated Raf --> activation of MAP kinases --> phoshorylate transcription factors, enzymes... many effectors 4. Ras inactivates itself by cleaving GTP to GDP
47
what is the AKT system for on a receptor tyrosine kinase
insulin signalling
48
what is the ras-raf-MAP kinase ligand?
growth factors
49
what happens after Ras binds Raf in an RTK
then you have the MAP kinases all phosphorylate
50
what is the 2nd messenger in a Ras-Raf-MAP RTK?
no typical 2nd messenger
51
receptor tyrosine kinase signalling options: PI-3 kinase - AKT system what is the signalling for and what are the steps?
-insulin signaling 1. RTK activated --> activates phosphoinositide-3-kinase (PI3K) 2. PI3K attaches another phosphate to PIP2 (membrane lipid) --> PIP3 3. PIP3 accumulates and forms "lipid" rafts in the membrane --> PIP3 is a 2nd messenger 4. Akt and PDK1 (both kinases in the cytosol) accumulate and cluster together at the site of the PIP3 rafts --> PDK1 becomes activated by PIP3 5. when PDK1 is activated, it activates Akt by phosphorylating it 6. Akt is the effector -many intracellular targets (also regulated on/off by others)
52
what is the second messenger in RTK PI3 kinase and AKT system? and what does it form
PIP3 is second messenger and forms lipid rafts (for PDK1 and Akt)
53
PI3 kinase role in cell signalling - what are its products?
converts many phospholipids into PIP3
54
what converts PIP2 to IP3 and DAG in Gq activation
PLC (phosholipase C)
55
what is the effector molecule in the PI3K Akt system?
Akt
56
what does nitric oxide do to smooth muscles
relaxes them
57
how is nitric oxide produced
by nitric oxide synthase (NOS) on L-arginine because of increase in cytosolic calcium concentration activate NOS
58
what role can nitric oxide play in cell signalling
act as 2nd messenger
59
nitric oxide
-key mediator that relaxes smooth muscle in a wide variety of blood vessels and visceral organs -small hydorphobic gas --> diffuses quickly, can effect many cells -produced enzymatically by the action of nitric oxide synthase (NOs) on L-arginine - increased cytosolic calcium can also activate NOs -nitric oxide rapidly degrades (reacts with oxygen and water) -2nd messenger than can diffuse; only local effects bc quickly degraded free radical
60
nitric oxide mediated signalling
1. cytosolic calcium increases 2. intracellular calcium activates nitric oxide synthase 3. nitric oxide synthase produces nitric oxide from L-arginine 4. nitric oxide binds and activates guanylyl cyclase (GC) --> production of cGMP (secondary messenger) from GTP 5. elevations of cytosolic cGMP activated a protein kinase (usually PKG) -changes in cellular activity due to PKG activity -disengage myosin from actin in smooth muscle= relaxation
61
nitric oxide; what does it use for energy and what 2nd messenger is produced
GTP --> cGMP

BMS100 test 1 (24 decks)

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