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Test 4 MCM Leesy > B2.084 - Cellular Signaling > Flashcards

B2.084 - Cellular Signaling Flashcards

1
Q

What are the components of G protein coupled receptor signaling

A

G protein coupled receptors
Heterotrimeric G proteins
Guanine nucleotide (GTP, GDP)

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2
Q

How do you turn on G coupled receptor signaling

A

Ligands stimulate binding of guanine nucleotide GTP to heterotrimeric G proteins

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3
Q

How do you turnoff G protein coupled receptor signaling

A

Hydrolysis of GTP to GDP; prevent re-binding of GTP to heterotrimeric G proteins

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4
Q

What are some clinical examples of G protein coupled receptor signaling

A

Fight or flight response
Beta blockers
Cholera
Jansens metaphysical chondrodysplasia

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5
Q

What are the components of second messenger signaling

A 
Adenylate cyclase, cAMP
Calcium
ER
inositol triphosphate (IP3)
DAG
Phospholipase
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6
Q

How is second messenger signaling turned on

A

G protein activation

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7
Q

How is second messenger signaling turned off

A

Down regulate G protein signaling

Degradation and/or sequestration of second messengers

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8
Q

What are some medical examples of second messenger signaling

A

Cholera, Cushing’s syndrome

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9
Q

In GPCR signaling a lingand binds and causes

A

Conformational change in the receptor which translates to the heterotrimer

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10
Q

In GPCR conformational change in the heterotrimer leads to the promotion of

A

Nucleotide exchange which causes activation

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11
Q

In GPCR nucleotide exchange is followed by what

A

GTP-alpha and beta gamma subunits dissociate and interact with effector molecules

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12
Q

In GPCR what do the effectors do

A

Bind active G protein subunits and trigger downstream signaling events

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13
Q

In GPCR signal duration is regulated by what

A

How long GTP remains bound

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14
Q

What intrinsic factor activity helps regulate how long GTP stays bound

A

GTPase

Hydrolyzes GTP to GDP

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15
Q

What helps accelerate the desensitization of the G protein?

A

GTPs activating proteins (GAPs)

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16
Q

Free beta gamma subunits recruit GRKs for what purpose

A

GRKs phosphorylates only ligand occupied GPCRs

17
Q

What do phosphorylated GPCRs do?

A

Recruit and bind arrestins

18
Q

Phosphorylated arrestin bound GPCRs cant do what

A

Interact with heterotrimer, the G protein activation cycle is broken

19
Q

What happens to the Arr bound GPCR

A

Its internalized and degraded

Or

Dephosphorylated and recycled to the cell surface

20
Q

How do beta blockers work

A

They bind norepinephrine and epinephrine, inhibiting the fight or flight response. This lowers blood pressure and has a calming effect

21
Q

How does vibrio cholerae work

A

The bacteria targets the small intestines and secretes a toxin that is internalized by the cell.

22
Q

What is the cholera toxin

A

An ADP ribosyl transferase that ADP-ribosylates Arg201 of the G alpha subunit.

23
Q

What ADP ribosylated G alpha subunit cant do what

A

Hydrolyze GTP, this causes the G protein to be always active.

24
Q

What is one of the most common G protein effector molecules

A

Adenylate cyclase

25
Q

What does AC do

A

Converts ATP to phyrophosphate and the second messenger cAMP

26
Q

What is AC activated by

A

G alpha

27
Q

How does cAMP affect PKA

A

It binds to the regulatory subunit of the PKA allowing the catalytic subunit to interact with things

28
Q

What is PKA

A

A prominent second messenger depended protein kinas

29
Q

Active PKA causes what

A

Increased transcription, phosphorylation of a ton of stuff

30
Q

What gets rid of cAMP

A

Phosphodiesterase (PDE)

31
Q

What is PLC

A

Phospholipase C, another common G protein effector

32
Q

What is PLCs function

A

Its a lipase that cleaves PIP2 into DAG and IP3

33
Q

What do DAG and IP3 do

A

PCK binds to DAG activating the kinase

IP3 binds to receptors on the ER leading to Ca release

34
Q

What is a critical feature of signal transduction

A

Signal amplification

35
Q

How does the phenotype of the cholera toxin come about

A
  1. ) The toxin ADP ribosylates Arg201 of G alpha subunit.
  2. ) This makes the G protein always active.
  3. ) Because it’s always active there’s more cAMP being produced, leading to PKA activity,
  4. ) increased PKA activity leads to phosphorylation (activation) of CFTR channel leading to secretion of Cl —> Na+ —>water into intestinal lumen
36
Q

What causes Cushing syndrome

A

Excess cortisol production

37
Q

What mutation causes Cushing syndrome

A

L206R on the catalytic subunit of PKA, this blocks its reassociated with regulatory subunits leading to increased PKA which leads to increased cortisol

Test 4 MCM Leesy (6 decks)

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