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Biochem 2 > Biosignalling > Flashcards

Biosignalling Flashcards

1
Q

Ligands and receptors interact in which way with each other?

A

Non covalently

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2
Q

What are the 6 features of signal transduction?

A
  1. Amplification
  2. Modularity
  3. Desensitization/Adaption
  4. Specificity
  5. Integration
  6. Localization
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3
Q

What is integration?

A

Ability of the system to receive multiple signals and produce a unified response

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4
Q

What is specificity?

A

Receptors have specific ligands

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5
Q

How can a desensitized system become resensitized?

A

When the stimulus falls below a certain threshold

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6
Q

What is an effector?

A

Selectively binds to protein and regulates its activity, act as ligands, can increase/decrease enzyme activity

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7
Q

How many transmembrane alpha helices do GCPR’s have?

A

7

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8
Q

What are the 3 essential components of GPCR’s?

A
  1. Plasma membrane protein receptor with 7 alpha helices
  2. G protein (cycles between active/inactive)
  3. Effector Enzyme/ion channel regulated by G protein
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9
Q

What is the 1st messenger for GPCR’s?

A

Extracellular ligand

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10
Q

When is a G protein active?

A

When it’s GTP bound

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11
Q

When G protein attaches to GTP, does it stay on the receptor?

A

No, dissociates, then binds to effector

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12
Q

What is the 2nd messenger in GCPR’s?

A

Cytosolic metabolite/inorganic ion

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13
Q

What are the ligands for andrenergic receptors? (GCPR’s)

A

Epinephrine

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14
Q

What is an agonist?

A

Natural ligand, produce effect of natural ligands

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15
Q

What is an antagonist?

A

Bind receptor without effect, block agonists

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16
Q

What is the stimulatory G protein? (Gs)

A

Activates the effector

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17
Q

In andrenergic receptors, what is the Gs?

A

Gsalpha

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18
Q

What activates adenylyl cyclase in andrenergic receptors?

A

Gsalpha

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19
Q

What catalyzes the formation of cAMP in andrenergic receptors?

A

Adenylyl Cyclase

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20
Q

What does cAMP activate?

A

Protein Kinase A

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21
Q

When concentration of cAMP is low, is PKA active or inactive?

A

Inactive

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22
Q

When PKA is active, what is the cAMP concentration?

A

High

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23
Q

How does adenylyl cyclase create cAMP?

A

Removes 2 p’s off of ATP to create cAMP

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24
Q

What are the 3 ways signals can be terminated? (andrenergic receptors)

A
  1. Epinephrine concentration goes below threshold
  2. Hydrolysis of GTP bound to G alpha-end cAMP production
  3. cAMP is hydrolyzed to 5’AMP by cyclic nucleotide phosphodiesterase
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25
Q

What does cyclic nucleotide phosphodiesterase do?

A

Hydrolyze cAMP to 5’AMP

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26
Q

What are GAPs?

A

GTPase Activator Proteins: Stimulate GTPase activity=more rapid inactivation of G protein

27
Q

What are RGS?

A

Regulators of G protein signalling

28
Q

What are the 4 classes of Galpha?

A
  1. Gsalpha: Stimulates AC
  2. Gialpha: inhibits AC
  3. Gqalpha: Stimulates PLC
  4. G12/betagamma: Regulate actin cytoskeleton
29
Q

What happens when Gi binds to AC?

A

Hormones that induce Gi binding inhibit AC

30
Q

How are andreneric receptors desensitized?

A

Protein kinase phophorylates receptor on intracellular domain that normally interacts with Gs

31
Q

What does BARK do?

A

Binding of epinephrine triggers dissociation of Gsby from Gsalpha-Gsby recuits BARK=phosphorylates Ser residues near COOH

32
Q

How are BARK and B-arrestin involved in GPCRs?

A

Desensitization-

  1. Binding of epinephrine triggers dissociation of Gsby from Gsalpha-Gsby recuits BARK=phosphorylates Ser residues near COOH
  2. Phosphorylation creates binding site for B-arrestin-blocks receptor sites that interact with Gs
  3. Receptor taken into cell via endocytosis-dephosphorylated=resensitized
33
Q

How does PKA contribute in desensitization of GPCRs?

A

PKA activated by high cAMP phosphorylates and activates BARK

34
Q

What are AKAPS?

A

A Kinase binding Protein-localize PKA

35
Q

GPCR coupled with PLC uses what kind of signalling?

A

IP3 and Ca2+

36
Q

What does PLC do?

A

Catalyzes cleavage of membrane PIP2 to and DAG. Activated by Gs.

37
Q

Which 2nd messenger opens Ca2+ channels?

A

IP3

38
Q

What does high cytosolic Ca2+ concentration do?

A

Trigger activation of PKC

39
Q

What is the extracellular domain of TKR usually made of?

A

Cys, Leu

40
Q

What are the 2 pathways TKR signals with?

A

MAPK (rigrrmet) and PIP3

41
Q

Where is the enzyme active site on TKRs?

A

Cytoplasmic face-protein kinase

42
Q

What does riggRRmet stand for? (Insulin receptor)

A 
r- Receptor
i- IRS
g- grb2
R- RAS
R- RAF
m-MEK
e-ERK 
t- Target
43
Q

What does ERK do? (RTK)

A

Enters nucleus and phosphorylates transcription factors, activating them

44
Q

Which molecule does PIP3 path branch at from MAPK?

A

Grb 2 is not the only protein IRS1 associates with-also PI3K

45
Q

What does PI3K do?

A
  1. Binds to active IRS1

2. Phosphorylates PIP2 to PIP3 using ATP

46
Q

What are the 2 paths in insulin PIP3 signalling?

A

A: Activated PKB phophorylated GSK3=inactive, can’t inactive GS=glycogen synthesis accelerated
B: PKB stimulates GLUT4 to move to plasma membrane and open= more glucose uptake

47
Q

What does GSK3 do?

A

Phophorylated glycogen synthase (GS), making it inactive.

48
Q

Phosphorylated IRS1 provides binding sites for which 2 adaptor proteins?

A

Grb2 and PI3K

49
Q

What does PIP3 do in insulin signalling?

A

Allows PKB to dock, which is then phosphorylated by PDK1

50
Q

When GSK3 is phosphorylated, is it inactive or active?

A

Inactive.

51
Q

Kinases most commonly phosphorylate which amino acids?

A

Ser, Thr, Tyr

52
Q

What does polarized mean?

A

Cell is in resting membrane potential state.

53
Q

What does depolarized mean? What is the ion movement?

A

Inside becomes more positive, Na and Ca rush in

54
Q

What does hyperpolarized mean? What is the ion movement?

A

inside becomes more negative, Cl- and K+ rush out

55
Q

What is the ion movement when a signal travels through an axon?

A

Na+in, K+ out

56
Q

Why does Cl- move against the concentration gradient?

A

Moving due to electrical gradient instead.

57
Q

What acts as the 2nd messenger in neurons?

A

Ca2+

58
Q

When Ca concentration in neurons increases, what happens?

A

Triggers release of acetylcholine into synaptic cleft

59
Q

What happens when acetylcholine binds to its ligand gated receptor?

A

Opens channel, allowing cations (Na and Ca) to enter

60
Q

What percentage of nuclear receptors are not inside the cell?

A

5-10%

61
Q

Why is signal transduction for nuclear receptors usually slow?

A

Ligand must be hydrophobic and cross cell membrane via diffusion.

62
Q

How do nuclear receptor ligands travel around the body?

A

Bound to carrier proteins.

63
Q

What happens when the ligand binds to a nuclear receptor?

A

Receptor dimerizes with other receptor, and binds to hormone response elements (HREs)-then receptor attracts corepressors/coactivators

Biochem 2 (6 decks)

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