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Foundations 1 > Week 2 Signal Transduction 2 Lecutures > Flashcards

Week 2 Signal Transduction 2 Lecutures Flashcards

1
Q

what is signal transduction

A

the process by which extracellular signals effect a change in the internal working of a cell

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2
Q

why are there generally so many steps in signal transduction pathways? (3 potential reasons)

A

signals can be modified at each step, signals can be amplified, signals can be distributed to several parallel processes

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3
Q

how are signaling cascades relayed (3)?

A

enzyme activity, protein-protein interactions, second messengers

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4
Q

what are the three major classes of second messengers?

A

cyclic nucleotides (cAMP, cGMP), IP3/DAG, Calcium ions

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5
Q

why wont a cell survive in saline?

A

cells depend on signaling from their micro-environment of growth and survival. without these signals the cell dies

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6
Q

what explains why different cells respond differently to the same signal?

A

difference in receptor structure, or difference in internal signaling pathways

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7
Q

How do the following cell types respond to ACh? heart muscle cell, salivary gland, skeletal muscle cell

A

heart: decrease rate and force of contraction
salivary: increase secretion
skeletal: contraction

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8
Q

how are signals withdrawn?

A

the signaling molecule can be down-regulated (degraded) or the recepotr can be down-regulated (inactivated, reduced synthesis, internalized)

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9
Q

What is acetylcholinesterase?

A

enzyme normally found in the synapses between cholinergic neurons and muscle that degraged ACh

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10
Q

What causes Myasthenia Gravis? how can it be treated

A

body produces antibodies against ACh receptors. Treatment is an acetlycholinesterase inhibitor that increases the concentraiton of ACh to compensate for decreased receptors

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11
Q

What are some examples of immediate modifications to cells in response to signaling?

A

changes in cell shape or activity

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12
Q

what are some examples of long-term changes to cells in response to signlaing?

A

changes in growth rate or differentiation (things that require gene expression and protein synthesis)

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13
Q

what are the three types of extracellular signaling pathways

A

Cell-surface receptors, intracellular receptors, gases

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14
Q

describe the structure of GPCRs

A

extracellular ligand-binding domain, 7 transmembrane domain, intracellular domain that binds G-proteins

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15
Q

G-proteins are active when? inactive?

A

active when GTP bound, inactive when bound to GDP

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16
Q

What is the structure of lipid linked G-proteins?

A

trimeric: alpha, beta and gamma subunits

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17
Q

what are the steps involved in the GPCR pathway

A
  1. ligand binds GPCR causing confirmational change in the alpha subunit
  2. alpha subunit of G protein exchanges GDP for GTP (GTP is now attached)
  3. the alpha and beta/gamma subunits dissociate and move on to activate or inhibit target proteins
  4. GTP bound to alpha subunit is eventually hydrolyzed to GDP causing reassembly of alpha/beta/gamma
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18
Q

For each g-protein give the active unit and function:
Gs
Gi
Go

A

Gs: alpha, activates adenyl cyclase
Gi: alpha, inhibits adenyl cyclase
Go: beta/gamma, activates K channels; also phopholipase C

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19
Q

in general, enzyme linked receptors (RTKs) are involved with_____ that produce ______ effects on cells

A

GFs: cell growth, proliferation, differentiation, survival

long-term

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20
Q

what is the best example of an enzyme-linked receptor?

A

RTKs

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21
Q

what is a kinase?

A

an enzyme that post-translationally phosphorylates a target molecule

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22
Q

Tyrosine kinase phosphorylate which residue?

A

Tyrosine

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23
Q

Ser/Thr kinases phosphorlyate which residue?

A

Ser/Thr

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24
Q

what percent of human proteins are phosphorylated? what charge does phosphorylation add to a protein?

A

30%, negative charge

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25
Q

what is a phosphatase?

A

dephosphorylates molecules

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26
Q

describe the structure of RTKs

A

single pass transmembrane proteins with an extracellular receptor domain and an intracellular tyrosine kinase domain

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27
Q

Describe the steps in RTK signaling

A
  1. ligand binds causing alpha and beta RTK subunits to dimerize
  2. the subunits autophosphorylate each others Tyr residues
  3. activated tyrosine kinases bind SH2 domain-containing proteins
  4. various pathways proceed
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28
Q

where do we see ion-linked receptors? how are they opened/closed

A

transduction of neural signals. neurotransmitters bind to receptors that transiently open/close ion channels

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29
Q

how do intracellular receptors work?

A

small, hydrophobic molecules diffuse across plasma membrane and are capture by the intracellular receptors. the intracellular receptor then enters the nucleus where they can affect gene expression

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30
Q

how do small hydrophobic (intracellular receptor ligands) exist in plasma?

A

associated with a carrier protein becuase they cant exist in an aq environment by themselves

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31
Q

what is an example of a ligand for an intracellular receptor?

A

steroid hormones derived from cholesterol

32
Q

How does NO act as a signal molecule?

A

NO binds to and activates guanylyl cyclase which produces second messenger cGMP

33
Q

increased cGMP levels does what?

A

relaxes smooth muscle cells (NO indirectly causes vasodilation)

34
Q

how is NO synthesized?

A

from Arginine by the enzyme NO synthase

35
Q

Vasodilation has what impact on BP

A

Lowers it nogga

36
Q

how do erectile dysfunctions drugs work?

A

inhibits cGMP breakdown and cause continuous vasodilation. this ensures blood goes to genitals

37
Q

how is cAMP made? where is this enzyme located?

A

synthesized from ATP by adenylyl cyclase. located in the membrane

38
Q

how is cAMP degraded?

A

cAMP phosphodiesterase this enzyme is always active

39
Q

the actions of adenylyl cyclase (to produce cAMP) is stimulated by? inhibited by?

A

stimulated by Gs (GPCR, alpha subunit)

inhibited by Gi (GPCR, alpha subunit)

40
Q

what is the function of cAMP

A

cAMP can activate protein kinase A

41
Q

what is the fxn (2) of PKA?

A

PKA can phosphorylate protieins int eh cytosol or PKA can travel into the nucleus where it activates other proteins that regulate gene transcription

42
Q

E and NE bind which G-protein linked class of receptors?

A

adrenergic receptors

43
Q

what does the stimulation of heart adrenergic receptors do?

A

increase heart rate

44
Q

what are beta blockers? what are they used for?

A

antagonist of some adrenergic receptors that are used to treat hypertension

45
Q

how does Cholera toxin work?

A

cholera toxin adds ADP-ribose to the alpha subunit of Gs and prevent the hydrolysis of GTP to GDP. this causes excess cAMP and a massive flow of water into intestinal lumen.

46
Q

how is cGMP produced? degraded?

A

produced: guanlyly cyclase

broken down: cGMP phosphodiesterase

47
Q

Role of cGMP

A

important in smooth muscle relaxation and vasodilation

48
Q

what is PIP2

A

phoshpatidylinositol (a phospholipid on the inner leaflet of PM) with 2 phosphate groups attached

49
Q

what is the role of phospholipase C? how is it activated?

A

PLC breaks down PIP2 into DAG (remains in membrane) and IP3 free to roam cytosol. activated by a GPCR

50
Q

the products of PIP2 cleavage via phospholipase C are DAG and IP2, what are their roles

A

DAG: activates PKC which plays a role in phosphorylation/activation of other proteins

IP3: triggers opening of Ca channels in ER

51
Q

When talking about RTKs what are adaptors?

A

a protein that contains an SH2 domain and binds to RTK but only acts as a scaffold for other proteins to attach

52
Q

what is Ras, how is it activated?

A

a monomeric G-protein, activated downstream of RTK (RTK–>Adaptor protein–>Ras-activating protein–>Ras)

53
Q

What pathway does Ras activate?

A

the MAP-kinase cascade (MAP-kinase kinase kinase–>MAP kinase kinase–>MAP kinase). plays a role in cell proliferation. some MAP kinase pathways are activated by cell stress.

54
Q

mutations in Ras are seen in what % of all human cancer?

A

30%, Ras is an ocogene

55
Q

what is the role of PI-3 Kinase? how is PI-3K activated?

A

phosphorylates PIP2 to make PIP3. PI-3K is activated by Ras

56
Q

what are two enzyme-linked receptors that do not require long cascaded of signal proteins?

A

JAK-STAT pathway and TGF-Beta pathway

57
Q

what are cytokine recepotrs?

A

the collective name for JAK-STAT receptors, important in immunity and inflammation

58
Q

what is unique about the JAK-STAT pathway

A

the receptor does not have intrinsic kinase ability so it bind JAK, a cytoplasmic kinase

59
Q

describe the steps in the JAK-STAT pathway

A

cytokine binds receptor–> cytokine receptors dimerize and associated JAKs cross phosphorlyate each other–>activated receptors recruit and phosphorylate STAT–>STAT enter nucleus and affect gene expression

60
Q

What type of enzymatic activity do TFG-beta receptors have

A

Ser/The kinase

61
Q

what is the signal cascade for TGF-Beta receptors?

A

TGF-Beta binds TFG-Beta receptor–>receptor phosphorylates itself and becomes active–>activated TGF-beta activated intracellular SMAD–>SMAD travel to nucleus and regulate gene expression

62
Q

what % of our genes encode protein kinases

A

2%! wow thats alot

63
Q

do all signaling pathways act independtly of each other?

A

no there is extensive cross talk among signaling pathways

64
Q

Beta-adrenergic receptors are what type of receptor? what is their ligand?

A

GPCR. E/NE

65
Q

what is the role of B-adrenergic receptors?

A

play a predominant role in regulating contractility of heart muscle. there are atleast nine adrenergic receptors in the heart, but B-AR are most prominant in regulating heart fxn

66
Q

what type of G-protein do B-ARs associate with?

A

Gs. Recall: Gs activates adenyl cyclase and the PKA pathway. PKA phophorylates cytoplasmic targets that regulate contractility, relxation, and Heart Rate

67
Q

what is desensitization? which type of receptor is it seen in?

A

the minimization of receptor activity due to continous agonist binding. GPCRs

68
Q

Why is desensitization helpful?

A

there are conditions such as chronic stress and disease in which high levels of E/NE are expressed. Desensit. prevents continual B-AR activation

69
Q

what are the three mechanisms in which GPCR can be desensitized?

A

down regulation (decrease receptor synthesis or degrade), sequestration (internalization of receptor), inactivation (phosphorylation)

70
Q

What is the role of GRKs? when is the only time GRKs work?

A

phosphorylate GPCRs and inactivate them. GRKs can only phosphorylate GPCRs that have been activated by ligand binding

71
Q

what occurs after GRKs phosphorylate GPCRs?

A

Arrestin binds to GPCR rather than a G-protein (arrestin is involved in other signaling pathways

72
Q

what effect does heart failure have on beta-AR signaling? how can you treat heart failure?

A

damage to heart causes an increase in Sympa NS and produces chronically high levels of E/NE. This desensitizes beta-ARs due to up regulation of GRKs. this further weakens the heart. paradoxically treating heart failure patients with beta blockers improves beta-AR signaling

73
Q

insulin receptors are what type of receptor?

A

RTK

74
Q

what is the main fxn of the insulin pathway?

A

triggers vesicles with GLUT4 in their membrane to fuse with the plasma membrane thus increasing glucose uptake in cells

75
Q

what is the role of PTEN

A

PTEN is a phosphatase that converts PIP3 to PIP2

76
Q

the activated insulin receptor activates what two pathways?

A

MAP kinase signaling pathway and PI-3K signaling pathway

77
Q

much of the effects of the PI-3K pathway is due to downstream activating of….what are these effects?

A

AKT. cell cycle, apoptosis, cell survival, glucose metabolism, immune response, neural development

Foundations 1 (65 decks)

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