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MAMS BCH Exam III > Spencer Cell Signaling LN > Flashcards

Spencer Cell Signaling LN Flashcards

1
Q

Juxtacrine

A

Direct physical contact between cells
- surface protein/receptor interactions

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2
Q

Endocrine on/off response speed, affinity, type of molecule

A

Hormones
- slow on/off
- very high affinity

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3
Q

Paracrine on/off response speed, affinity, type of molecule

A

Local mediators (growth factors, cytokines)
- rapid response
- low-high affinity

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4
Q

Synaptic on/off response speed, affinity, type of molecule

A

NTs
- very low affinity
- very rapid response

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5
Q

Autocrine on/off response speed, affinity, type of molecule

A

Large proteins (GFs, Cytokines)
- Low to high affinity
- Rapid response

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6
Q

Types of 1st messengers

A

NTs, Hormones, GFs, Cytokines

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7
Q

Are NTs hydrophilic or hydrophobic

A

Hydrophilic

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8
Q

Hydrophilic vs Hydrophobic hormones

A

Hydrophilic: usually charged, interact with cell-surface receptors
Hydrophobic: membrane permeable, interact with intracellular receptors

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9
Q

Growth Factors range

A

Long range

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10
Q

Cytokines range

A

local range, coordinate immune response

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11
Q

Agonist

A

Ligand that activates normal response
- inhibitor or excitatory

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12
Q

Antagonist

A

Ligand that induces no response
- blocks normal response

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13
Q

Effector

A

Intracellular receptor that responds to activated receptors and generates 2º messengers

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14
Q

Coupling

A

Transmits signal from activated receptor to effector

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15
Q

Adaptor

A

Intracellular protein that lacks enzymatic activity but contains several domains that mediate protein-protein interactions

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16
Q

What are the 2 molecular switches

A

1) Protein phosphorylation
2) Guanine NT binding (G protein cycle)

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17
Q

Activation of G protein cycle

A

GDP is exchanged for GTP
- assisted by receptor if trimeric
- GEF (Guanine NT EF) for monomeric

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18
Q

Inactivation of G protein cycle

A

GTP hydrolyzed to GDP using GTPase
- If monomeric, requires GAPs (GTPase activating proteins)

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19
Q

3 receptor criteria

A

1) Specificity
2) Appropriate binding affinity
3) Transmission of message via further modification of signaling cascade

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20
Q

2 receptor classes

A

1) Intracellular
- causes long-lasting changes
- displaces HSP
2) cell-surface receptors
- triggers an increase in 2º messenger concentration

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21
Q

GPCR mechanism

A

1) Ligand binds (activates up to 100)
2) conformational change exposes regulatory site, allowing G-protein to bind
3) GDP exchanged for GTP, causes G protein dissociation
4) alpha subunit binds to membrane-bound enzymes, activates 2º messengers
5) Intrinsic GTPase activated, hydrolyzing GTP causing release from enzyme
6) G protein alpha subunit reassembles with beta gamma complex

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22
Q

Affinity of ligands for GPCR?

A

Low to high affinity

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23
Q

How is GPCR terminated

A

Phosphorylation of Ser/Thr on C-terminal tail

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24
Q

What 1º messengers does the GPCR react to?

A

NTs, hormones, cytokines (especially chemokine)

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25
Q

GPCR structure

A

N-terminal outside, C-terminal inside, 7 transmembrane subunits

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26
Q

Structure of GPCR alpha subunit

A

Hydrophilic with a lipid membrane anchor

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27
Q

beta-gamma complex

A
  • hydrophobic
  • covalently attached lipid anchor
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28
Q

4LOKO example

A

EtOH
1) EtOH binds to allosteric site
2) prolonged opening of GABA channel
3) increased negative membrane potential
4) suppression of neural activity

Caffeine
1) Blockage of binding site (antagonist)
2) cancellation of Adenosine effect
3) increased neural activity
4) blood vessel construction, epi release, increased alertness

Both
5) increased dopamine release

29
Q

2 types of enzyme-linked receptors

A

1) Tyrosine Kinase
2) Serine/Threonine Kinase

30
Q

Tyrosine Kinase receptor mechanism

A

1) Ligand binds to RTK causing dimerization and activation of kinase domain
2) Active RTK autophosphorylates Tyrosine residues
3) Phosphorylation causes binding and activation of adaptor proteins (cascade)

31
Q

MAP Kinase cascade

A

Example of Tyrosine Kinase Receptor triggered cascade
1) Adaptor protein binds RAS-activating protein
2) Activation of RAS via GDP to GTP
3) RAS attracts MAPKKK
4) MAPKKK activated by membrane
5) MAPKKK to MAPKK via ATP
6) MAPKK to MAPK by ATP
7) MAPK phosphorylates targets

32
Q

Receptor Serine/Threonine Kinase

A

1) Autophosphorylation causes type II homodimer to become constitutively active
2) Ligand pulls Type I to combine with Type II
3) Ser/Thr becomes phosphorylated
4) SMAD binds to Type I and becomes phosphorylated
5) SMAD unfolds and activates
6) SMAD dimerizes with other SMAD, exposes NLS
7) Alters gene expression

33
Q

Traits of enzyme-linked receptors

A

Binding activates cytoplasmic enzyme activity
- Endocrine, Paracrine
- Hormones, Growth Factors
- Very high affinity

34
Q

How do enzyme-linked receptors terminate

A

Receptor-mediate endocytosis
- down-regulation

35
Q

Traits of cytokine-linked receptors

A

Binding of ligand causes association and activation of cytoplasmic enzymes
- paracrine, autocrine
- cytokines, GFs
- low to high binding affinity

36
Q

How are cytokine-linked receptors terminated

A

Via receptor-mediated endocytosis and protein phosphatases

37
Q

JAK-STAT Pathway mechanism

A

type of cytokine receptor
1) JAK attracted to Pro-rich regions on transmembrane peptides
2) Cytokine binds causes association of subunits and JAK activation
3) JAK Tyr + subunit phosphorylation
4) STAT dimer binds to Tyr
5) STAT phosphorylated
6) STATS dissociate, dimerize, expose NLS

38
Q

Ebola virus mechanism

A

Normally
1) STAT1 dimer binds to Importin a5/ß complex
2) ß brings Importin complex through nuclear pore
3) Ran-GTP dissociates Importin complex
4) STAT1 causes expression of antiviral immune response

Ebola effect
- VP24 ebola protein displaces STAT1 to form Importin complex

39
Q

Types of 2º messengers

A

Ions: Ca2+
H2O-soluble molecules: cAMP, cGMP, IP3
Membrane-associated molecules: DAG, Arachidonic acid, PIP3

40
Q

Ca2+ concentration which means the cell is quiet

A

10^-7 M or less

41
Q

Ca2+ concentration which means the cell is active

A

10^-6 M or greater

42
Q

Ca2+ removal mechanisms

A

1) NCX Na+/Ca2+ exchanger
2) PMCA Ca2+ ATPase
3) SERCA

43
Q

NCX mechanism

A

Gets most Ca2+ out
- Ca2+ out, 3 Na+ in
- low affinity, high rate

44
Q

PMCA

A

Gets rest of Ca2+ out
- ATP pushes Ca2+ into protein
- eversion, Ca2+ out
- high affinity, low rate

45
Q

Ca2+ addition mechanisms

A

1) Ligand-gated ion channel
2) Voltaged-gated Ca2+ channel
3) RyR
4) IP3R

46
Q

RyR

A

2 Ca2+ bind to cause more Ca2+ release

47
Q

IP3R

A

IP3 and Ca2+ bind to release Ca2+ from ER

48
Q

CICR

A

Ca2+-induced Ca2+ release

49
Q

Creation of cAMP

A

ATP dephosphorylated by Adenylate Cyclase, creation of phosphodiester bond

50
Q

Degradation of cAMP

A

cAMP phosphodiesterase uses H2O to create 5’-AMP

51
Q

Regulation of cAMP

A

Regulated by balance of G proteins
- G proteins can be inhibitory or excitatory

52
Q

Cholera

A

Binding of ADP-ribose causes constitutive activation of adenylate cyclase
- increase in cAMP, excessive loss of H2O, shock

53
Q

Pertussis

A

Prevents activity of inhibitory G protein
- increased PKA, high insulin producing low glucose, high histamine sensitivty

54
Q

cGMP creation

A

Guanylate cyclase creates phosphodiester bond in cGMP

55
Q

cGMP degradation

A

cGMP phosphodiesterase uses H2O to degrade it to 5’-GMP

56
Q

Effect of NO in cGMP

A

Increases cGMP production by binding to soluble guanylate cyclase

57
Q

Effect of ANF (hormone)

A

Increases cGMP production by binding to membrane Guanylate cyclase

58
Q

Effect of increase cGMP

A

Production of PKG, phosphorylation of target proteins

59
Q

Phospholipid sources of 2º messengers

A
  • Phosphatidylcholine
  • Phosphoethanolamine
  • Phosphatidylinositol
60
Q

Enzyme that converts PI to PIP

A

PI-4 kinase

61
Q

Enzyme that converts PIP to PIP2

A

PI-5 Kinase

62
Q

What is special about PIP2

A

Contains 3 PO4- groups, major substrate for producing 2º messengers

63
Q

Types of 2º messengers derived from phospholipids

A

IP3, DAG, Arachidonic acid, PIP3

64
Q

What is the largest GPCR subunit?

A

Alpha subunit

65
Q

Which subunit contains the GTP/GDP binding site?

A

Alpha subunit

66
Q

Which subunit determines the G protein subtype?

A

Alpha subunit

67
Q

Do RTKs and Ser/Thr Kinases have intrinsic enzymatic activity?

A

Yes, binding activates intrinsic enzymatic activity of cytoplasmic domain

68
Q

Do cytokine receptors have intrinsic enzymatic activity?

A

No

MAMS BCH Exam III (12 decks)

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