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BIO 317 > 21 - Signaling Scaffolds and Cross-Talk > Flashcards

21 - Signaling Scaffolds and Cross-Talk Flashcards

1
Q

In fibroblasts, what does sustained ERK signaling lead to?

A

Proliferation

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2
Q

In fibroblasts, what does transient ERK signaling lead to?

A

Quiescence

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3
Q

In PC12 cells, what does sustained ERK signaling lead to?

A

Differentiation

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4
Q

In PC12 cells, what does transient ERK signaling lead to?

A

Proliferation

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5
Q

In yeast, what does sustained ERK signaling lead to?

A

Filamentous growth

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6
Q

In yeast, what does transient ERK signaling lead to?

A

Mating

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7
Q

How does cAMP function in the ERK pathway?

A

It inhibits Raf-1 and activates B-raf

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8
Q

Does cAMP lead to sustained or transient ERK activation?

A

Sustained ERK activation

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9
Q

What is MP1?

A

A signaling scaffold protein bound on the signaling endosome

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10
Q

Where is MP1 found?

A

At the endosome

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11
Q

Which proteins bind to MP1?

A

MEK, ERK, and p14

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12
Q

What is KSR?

A

A signaling scaffold protein bound at the cell membrane

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13
Q

Where is KSR found?

A

At the cell membrane

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14
Q

Which proteins bind to KSR?

A

Raf-1, MEK, and ERK

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15
Q

What type of signaling is MP1 associated with?

A

Sustained ERK signaling

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16
Q

What type of signaling is KSR associated with?

A

Transient ERK signaling

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17
Q

Which scaffolding protein works on cytosolic targets?

A

KSR

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18
Q

Which scaffolding protein works on nuclear targets?

A

MP1

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19
Q

What is the advantage of KSR?

A

Brings Raf, MEK, and ERK together at the cell surface in proximity of Ras for specific signaling

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20
Q

Where is Ras found in the cell?

A

At the cell surface

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21
Q

True or false: signaling scaffolds allow for signal amplification

A

True: they can amplify the signal, even in the presence of phosphatases

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22
Q

How can signaling scaffolds lead to signal amplification?

A

They can block the proteins from being inactivated (blocking phosphatases)

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23
Q

How does ERK interact with KSR?

A

It can phosphorylate the site where Raf binds, preventing it from binding to the scaffold

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24
Q

What is the significance of the ERK interaction with KSR?

A

Allows for a timer function of the scaffolding system to turn on or off

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25
Q

What happens if KSR is mutated to not have pERK sites?

A

There will be sustained ERK signaling

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26
Q

How come mutation of KSR to the pERK sites leads to sustained ERK signaling?

A

There is no timer function to stop Raf from signaling to ERK

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27
Q

What happens to 14-3-3 in non-stimulated cells?

A

They keep KSR and Raf in the cytoplasm, and block the catalytic A and C units

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28
Q

What happens to 14-3-3 in stimulated cells?

A

They displace, allowing KSR and Raf to localize to the cell membrane, and allow the A and C units to lead to MEK/ERK signaling

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29
Q

What is 14-3-3?

A

A scaffold protein for KSR and Raf

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30
Q

What does the PH domain bind to?

A

PIP3

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31
Q

What proteins are brought together by PH domains?

A

PDK1 and Akt

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32
Q

True or false: PIP3 is not a second messenger

A

False: it is a structural organizing center

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33
Q

How does Akt get activated?

A

By binding to PIP3, exposing Thr308, which can be phsophorylated by PDK1

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34
Q

Which enzyme turns PIP2 into PIP3?

A

PI3K

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35
Q

Which enzyme turns PIP3 into PIP2?

A

PTEN

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36
Q

What happens if PH domains are disrupted?

A

This can lead to oncogenic activation of Akt

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37
Q

What is Gab1?

A

An organizing molecule (similar to PIP3)

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38
Q

What molecules can bind to Gab1?

A

PLC-gamma, PI3K, SOS, GRB2, and the receptor

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39
Q

What effects can be mediated by Gab1?

A

Cell proliferation, adhesion, motility, and survival pathways

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40
Q

What pathways can be mediated by Gab1?

A

Ras/Ref/MEK/ERK, Ras/Rac/PAK, FAK, and Akt/mTOR

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41
Q

True or false: Gab1 can only mediate sustained MAPK activation

A

False: it can also mediate transient MAPK activation through Ras

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42
Q

True or false: Gab1 can only mediates transient MAPK activation

A

False: it can also mediate sustained MAPK activation through SRC and PLC-gamma

43
Q

How does Gab1 create a positive feedback loop?

A

It recruits more PI3K, leading to more PIP3, leading to more recruitment of Gab1

44
Q

What were the first anchoring proteins described?

A

AKAPs

45
Q

What does AKAP stand for?

A

A kinase anchoring protein

46
Q

What proteins binds to all AKAPs?

A

PKA

47
Q

What is the purpose of the many isoforms of AKAPs?

A

They localize at different areas of the cell

48
Q

What are some examples of subcellular locations where AKAPs can localize PKA?

A

Nuclear membrane, centrosome, golgi, etc.

49
Q

Besides PKA, what can AKAPs localize?

A

Different signaling components downstream or upstream of that specific PKA

50
Q

What is the relationship between AKAPs and cAMP?

A

Each AKAP has a specific regulation on a local loop of cAMP

51
Q

How can AKAPs bind many different signaling components together?

A

They have different binding sites for effectors, PDEs, and PKA

52
Q

True or false: there are few diseases that involve a mutated AKAP

A

False: there are a variety of diseases associated with mutated AKAPs

53
Q

How specific are diseases involving AKAP mutations?

A

Tissue specific and substrate specific

54
Q

How can AKAP mutations in cardiomyocytes lead to cardiovascular disease?

A

This can prevent the cardiomyocyte from releasing calcium properly, reducing the effectiveness

55
Q

How can AKAPs lead to convergence of signaling?

A

AKAPs can bind to both PKA and PKC, leading to a convergence of signaling

56
Q

How can AKAPs lead to crosstalk?

A

They can bring together various kinds of signaling molecules that have common substrates

57
Q

What is an example of crosstalk mediated by AKAPs?

A

PKA and PKC can both interact with calcium/calmodulin or the muscarinic receptor, leading to crosstalk

58
Q

What does ARMS stand for?

A

Ankyrin repeat-rich membrane-spanning scaffold protein

59
Q

Where are ARMS found?

A

Embedded within the cell surface

60
Q

What proteins can bind to ARMS?

A

The cytoskeleton, Trk endosomes, and FRS2 (sustained ERK activation)

61
Q

How can ARMS regulate synaptic transmission?

A

By bringing together Trk, ephrin, and AMPAR receptors

62
Q

What is the structure and function of ARMS?

A

Large scaffold proteins to bring many things together

63
Q

What does PSD-95 stand for?

A

Post synaptic density 95

64
Q

What is PSD-95?

A

A scaffold protein found at the post synaptic density

65
Q

True or false: there are no diseases associated with mutation of PSD-95

A

False: there are a variety of diseases associated with mutation of PSD-95

66
Q

What are pleiotropic kinases?

A

Kinases that have multiple different functions

67
Q

How can scaffolds interact with pleiotropic kinases?

A

They can direct them to one specific pathway/function

68
Q

True or false: a scaffold protein cannot be an activating kinase

A

False: NIK functions as both an activating kinase and a scaffold protein

69
Q

What is the importance of the multiple domains in scaffold proteins?

A

Specificity and modularity

70
Q

What is meant by signaling pathways converging?

A

Signals from unrelated receptors can converge to activate a common effector

71
Q

What is meant by signaling pathways diverging?

A

Identical signals can diverge to activate a variety of effectors

72
Q

What is meant by signaling pathways crosstalking?

A

Signals can be passed back and forth between pathways as a result of crosstalk

73
Q

What is an example of crosstalk (with EGF and adrenaline)?

A

EGF and adrenaline can both converge onto CREB, with interactions between the pathways at Raf

74
Q

How can AC be a source of crosstalk?

A

In neurons, some AC need calcium to function

75
Q

What is an example of crosstalk in muscle fibers?

A

Phosphorylase kinase (activated by the adrenaline pathway) also needs calcium to function

76
Q

How has modern biology interacted with computational work?

A

Can be used to understand how large systems function within the cell

77
Q

What levels of networks are there (from highest to lowest)?

A

Organ/tissue networks, cellular networks, and molecular networks

78
Q

What questions (3) can be asked in network biology?

A
  1. How does a cell determine the final output?
  2. How do different cells translate differently?
  3. What does this imply for pharmacology?
79
Q

What questions (2) can be asked about drug use and networks?

A
  1. How does a cell in a dish translate to a cell in the body?
  2. How can off target effects be minimized?
80
Q

What are two strategies to study a molecule in a signaling network?

A

Looking at all the intermediates, or an input and output (with core processes and system control)

81
Q

What is the purpose of studying system controls in a network?

A

Can understand how perturbations of intermediates can affect the entire pathway

82
Q

True or false: three proteins arranged in the same network will have the same behavior

A

False: based on rate constants, the behavior can vary widely

83
Q

What are the different types of behaviors a negative feedback loop can have?

A

Steady state, drop to zero, oscillating, and dampened oscillations

84
Q

How does a threshold level affect a network?

A

Initial conditions below the threshold drop towards zero, while initial conditions above the threshold reach a steady state

85
Q

What determines the behavior of a negative feedback loop?

A

The rate constants of how the proteins interact with each other

86
Q

What is systems biology?

A

The study of different hierarchies of networks, and the relationships between the different levels of networks

87
Q

What is at the bottom of the systems biology triangle?

A

Genes, mRNA, proteins, and metabolites

88
Q

What is at the top of the systems biology triangle?

A

Large-scale organization

89
Q

What is in the middle (closer to the bottom) of the systems biology triangle?

A

Regulatory motifs and metabolic pathways

90
Q

What is in the middle (closer to the top) of the systems biology triangle?

A

Functional modules

91
Q

As you move up the systems biology triangle, what increases?

A

Universality

92
Q

As you move down the systems biology triangle, what increases?

A

Organism specificity

93
Q

What are the different (4) viewpoints of analyzing signaling networks?

A
  1. View from a particular input and analyzing the entire network as a stand alone system
  2. View from interactions between similarly acting inputs
  3. View from a particular signaling component and combining mini-networks of components
  4. View of the entire system
94
Q

What is an example of viewing a network as a stand along system with a particular input?

A

Studying neurotrophins and their pathway in the cell

95
Q

How can boundaries be established in a stand alone network?

A

Based on their functionality (PI3K, cytoskeleton, calcium, etc.)

96
Q

What is an example of viewing a network as interactions between similarly acting inputs?

A

Studying RTKs and the commonalities between them

97
Q

What is an example of viewing a network as a particular signaling component and combining mini-networks?

A

Studying just Rab1 signaling, and every interaction that it is involved in (inflow and outflow)

98
Q

What is an example of viewing a network as an entire system?

A

Studying hairballs that represent cellular signaling pathways

99
Q

What are hairballs?

A

Big tangled networks of signaling components

100
Q

What is the controversy surrounding hairballs?

A

They may be interesting computationally, but not biologically

101
Q

What is the goal of studying hairballs?

A

Create global networks that can take into account time and space differences

102
Q

What is the consequence of having nonlinear functions between proteins, genes, the environment, etc.

A

The relationships need to be simplified

103
Q

What is a diseasome?

A

An overlap between a gene network and a disease phenotype network

104
Q

What is the purpose of a diseaseome?

A

See how different genes and proteins interact in different diseases

BIO 317 (27 decks)

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