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Pharm Block 1 > Signal Transduction 2 > Flashcards

Signal Transduction 2 Flashcards

1
Q

EnZ linked receptors include

A

Tyrosine kinase linked
serine/threonine kinase-linked
Protein phsphatase-linked
Guanylyl cyclase linked

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2
Q

Two forms of Tyrosine kinase linked receptors

A

single protein w/ 1 transmembrane domain that dimerizes upon ligand binding
receptor has 2 subunits to form a tetramer upon binding

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3
Q

Tyrosine kinsae receptors have intrinsic

A

tyrosine kinase activity upon phosphorylation

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4
Q

EGF tyrposine kinase receptor is inactive as;

active as:

A

inactive a monomer

active as dimer

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5
Q

PDGF tyrosine kinsase receptor is incative as:

active as:

A

inactive as: monomer

active as: dimer

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6
Q

Insulin receptor is a tyrosine kinase receptor that is inactive as:
active as:

A

inactive as dimer

active as tetramer

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7
Q

Each TK receptor has ______ domain with tyrosine kinase activity

A

cytoplasmic

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8
Q

Activation of Tyrosine Kinase receptors is dimerized and activated by:

A

Trans-autophosphorylation

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9
Q

One dimer is activated by phosphorylation, it in turn phosphorylates the other unit back. Concept is called

A

Trans-autophosphorylation

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10
Q

After trans-autophosphorylation we bind:

A

intracellular molecules

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11
Q

Tyrosine kinase receptors are key for:

A

-regulation of cell proliferation and differentiation

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12
Q

ligands of tyrosine kinase include:

A

hormones like insulin

GFs like EGF, PDGF and VEGF

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13
Q

What receptors play imporant role in onogenesis and are targets of chemotherapies

A

Tyrosine kinase receptors

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14
Q

Receptors are first part of signal transduction and provide

A

specificiy

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15
Q

Receptors and their ligand are key, but we need what other guys to transduce a signal through cytoplasm into nucleus

A

intracellular signal molecules

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16
Q 
G proteins
Second messengers
Proteins kinases and Protein phosphates
Transcription factors 
are all examples of:
A

Intracellular signal molecues

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17
Q

Examples of intracell signal molecules

A

G proteins
Second messengers
Proteins kinases and Protein phosphates
Transcription factors

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18
Q

proteins that bind DNA and regulate transcription of gene

A

Transcription factors

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19
Q

CREB is :

A

cAMP response element biding protein

ubiquitous TF that activates many differnt genes

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20
Q

ubiquitous TF that activates many differnt genes

A

CREB

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21
Q

Myc, Fos, Jun are examples of

A

transcripion factors

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22
Q

What two things do signal transduction cascades regulate as far as TFs are concerend

A

Regulate it’s nuclear translocation and it’s ability to bind to DNA

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23
Q

What Regulates TF’s nuclear translocation and it’s ability to bind to DNA

A

signal transduction cascades

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24
Q

What do activated transcription factors do?

A

induce transcription by activating RNA polymerase–> get transcription of mRNA from target gene

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25
Q

Why do we want TF to activate RNA polymerase

A

bc then it will transcribe mRNA of target gene

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26
Q

Trend of TF;s is:
P’d by Protein Kinases will:
de-“d by protein phosphorylses will:

A

PKs will activate

PPs will inactivate

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27
Q

What aa do Protein kinases like to add P’s to

A

ser/threonine/tyrosine

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28
Q

PKA, PKC, Ca/calmodulin dependent kinase and MAP kinases are examples of

A

Serine/threonine specific PK’s

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29
Q

Tyrosine kinase-linked receptors like EGF and cytoplasmic kinases like Src and Abl are spefic for which protein kinase

A

Tyrosine specific

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30
Q

What kinases have dual specificiy and phosphorylate both tyrosine and threonine

A

MAP kinase kinases

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31
Q

The activity of a protein is often regulated by one/many kinases and phosphorlyases acting on a protein

A

MANY

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32
Q

What regulates activity of kinases and phosphatases

A

via second messengers

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33
Q

what does a protein kinase need to do it’s job

A

ATP

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34
Q

Phosphorylate protein is likely to

A

interact with dif effectors (more likely to then the d’Pd guy)

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35
Q

Small diffusible molecules generated in response to ligand-receptor interaction

A

second messengers

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36
Q

Second messengers will:

A

activate downstream effectors

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37
Q

cAMP is made when:

A

alpha sub activates adenylyl cylase : will will convert ATP–> cAMP

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38
Q

how does activated adnelylyl cyclase make cAMP

A

ATP–> cAMP

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39
Q

what does cAMP do?

A

acitates PKA

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40
Q

what activtes Protein kinase A

A

cAMP from activated adenylyl cyclase

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41
Q

DAG and IP3 are examples of

A

second messengers

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42
Q

How is DAG and IP3 made

A

Alpha-q will turn on Phospholipase C (PLC)–> PLC cleaves PIP2 to generate DAG and IP3

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43
Q

What do we generate from PIP2 and what enZ does this?

A

DAG + IP3 via PLC (acivated by alpha-q)

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44
Q

What does DAG do

A

activaes protein kinase C

45
Q

What turns on protein kinase C

A

DAG

46
Q

What does IP3 do?

A

IP3 binds to IP3 receptors on ER–> cuases Ca+ release

47
Q

What will cause Ca+ release from ER

A

IP3 binding to IP3 receptors

48
Q

Ca++ is a type of

A

secondary messenger

49
Q

how do we generate Ca++

A

opening ion channels

50
Q

What does Ca++ do intracellularly

A

binds to pretins and activates PKC adn other kinases and enZs

51
Q

cAMP binds to what units on PKA

A

binds to the R subunits and relases the active catayltic subs

52
Q

how mand cAMP’s does an adenylyl cylcase generate once activated?

A

MANY

53
Q

cAMP will result in _______ of signals

A

amplification

54
Q

What will phosphorylate CREB

A

PKA that was turned on by cAMP that was made from adenylly cylclase

55
Q

What will inhibit or turn off cAMP pathway

A

when aplha–i binds to adenylyl clycase and turns it off

56
Q

Metabolites of phospholipids activate:

A

Protein Kinase C

57
Q

GRPrs coulpled to _______ regulate the Inosotol-lipid pathway

A

G-alpha-q

58
Q

Pathway to activate DAG

A

Ligang–> to GPCR which then activates G-alpha-q via GTP binding–> PLC is actiaved via Galphaq–GTP binding

59
Q

What does PLC do

A

cleaves PIP2 into IP3 and DAG and DAG stays in membrane to activate PKC while IP3 goes on to release Ca+ from ER

60
Q

Ras, Rho, Rac, Rap and Rab are examples of

A

Monomeric G proteins

61
Q

these guys are activated by interacting w/ proteins known as guanine nucleotide exchange factots

A

Monomeric G proteins

62
Q

small molecular wt proteins, small GTPases and small GTP binding proetens or p21s are

A

Monomeric G proteins

63
Q

These guys are inactivated by interacting with proteins known as GTPase activating proteins

A

monomeric G proteins

64
Q

Monomeric G proteins are inactivated by interacting with proteins known as

A

GTPase activating proteins or GAPs

65
Q

KEy difference between hetertrimeric G proteins and monomeric G proteins

A

heterotrimeric activated by interactions with GPCR

monomeric activated by interaction with GEF

66
Q

A guanine nucelotide exchange factor is a

A

GEF

67
Q

This will activated mononumeric G proteins

A

GEF

68
Q

SOS is an example of a

A

GEF

69
Q

How are GEFS activated

A

when they are recruited to activated tryosine kinase linked receptors by adaptor proteins like GRB2

70
Q

process of activating GEF

A

ligan binds to dimerized tyrosine kinase receptor–> this will cause phosphorylation of an Adaptor–>The adaptor will then activate guanine nucleotide exchange factor

71
Q

GRB2 is an example of

A

an adaptor protein that will recuite GEF

72
Q

What happens when a GEF interacts with Ras-GDP

A

makes it release GDP and bind a GTP = Ras-GTP

73
Q

What does Ras-GTP do? how did it get the GTP

A

Ras-GTP will bind and singal other molecules

it got the GTP bc a GEF made it lose the old GDP and bind a GTP

74
Q

How can Ras go from Ras-GTP to Ras-GDP

A

it has intinisic GTPase activity

75
Q

How does Ras know when to hydorlyze it’s GTP?

A

Ras-GTP will associate with GAP (a GTPase activating protein) that induces Ras to hydrolyze it’s GTP

76
Q

What does GAP do

A

makes Ras-GTP hydorlyze it’s phosophate by activting the intrinsic GTPase activity Ras has

77
Q

Monomeric G proteins key for this signaling cascade

A

MAP or mitogen activated protein kinase sidnaling cascade

78
Q

How does the MAPK pathway work

A

Start with activationg of monomeric G protein–> activates MAP KKK–> P’s and activates MAP KK–> Ps and activates MAP kinase–> P the transcription factor

79
Q

Another way to phrase the MAPK pathway

A 
Ras-GTP gets a new GTP from GEF
Ras-GTP activates Raf
Raf P's MKK1
MKK1 P's ERK
ERK phosphorylates lots of TF's
80
Q

What is teh end result of the MAP kinase pathway

A

ERK gets’s P’d by MKK and will then phosphoyrlate a bunch of Transcription facots

81
Q

Mutations in this receptor can cause tumors that have abnormally high activity to promote tumorgenesis and metastasis

A

EGF receptor and Ras

82
Q

Mutation in EGF or Ras

A

promote tumorgenesis and metastasis

83
Q

What’s good cancer chemotherapeutic

A

agents inhibiting the signal by EGF receptor

84
Q

Gefeitinib and Erlotinib are used:

A

as tryosine kinase inhibitors by inhbiting singaling of EGF

85
Q

Efficiacy of Gefetinib and Erlotinib are enhanced by

A

presence of mutations on EGF receptor

86
Q

Gefetinib and Erlotinib decrease ________ in 80% patiens with mutated EGF receptor

A

lung tumor burden

87
Q

How well do gefetinib and Erlotinib work on patients without receptrion mutations in EGF?

A

only 10% help

88
Q

Population of individual more suspecitlbe to EGF receptor mutation leading to lung cancer (non-smoking induced)

A

Asian females with adenocarcinoma

89
Q

Cells need to be able to turne exctracell signals off, or there would be:

A

uncontrolled signaling

90
Q

Constituitive and uncontrolled signaling contributes to

A

cancer

91
Q

Many ______ are mutated signal molecules with promote uncontrolled, ligand-independent signaling

A

Oncogenes

92
Q

Turning off the signal

A

attenuation

93
Q

Attetuation

A

turning off signal at all levels each activated signal must go back to inactive state

94
Q

How do we accomplish attenuation

A 
ligan inactivation or dissociation from receptor
receptors dissocatie from proteins
Adaptor protein complexes dissociate
G protesin hyrodlyze GTP to GDP
Phospholyrlyation is done or undone
metabolize 2 messenger
ions sequesterd or pumped out
95
Q

Receptor mediated endocytosis is:

A

Adaption

96
Q

OCcurs when signaling system responds to intensity and frequency of stimulation; response is proportion to stimulus

A

Adaption

97
Q

If there is no ligand, receptors may:

A

not be localized in specific location on plasma membrane

98
Q

receptor mediated endocytosis to regulate number or amount of receptors that respond to signal
can promote degradation of both receptor and ligand

A

Adaption–because it’s induced by the binding of ligand to the receptor

99
Q

How does endocytosis of ligand-receptor complex occur

A

This is adaption

Done by migration of complexes to electron dense region of membrane coated in clathrin

100
Q

What happens once a receptor-ligand complex is engulfed in clarthin coated pit?

A

bind to CURL = vesicles with low pH that favor dissociation of the ligand from receptor

101
Q

Retroendocytosis

A

process of recycling ingested receptors

102
Q

Free receptor located in CURL can:

A

be recycled or

degraded

103
Q

Receptor desensitization is a form of

A

Adaption

104
Q

In ________ desensitization, signaling by stimulated receptor is attenuated

A

HOMOLOGOUS

105
Q

This occurs due to covalent modification of ligand-bound receptor

A

Homologous desensitization

106
Q

In receptor desensitization, signaling by the ______ is attenuated

A

stimulated
basically receptor gets stimulated, gets signaled to get phospohrlyed, then something binds to it, so as a reslt of it’s signaling, it gets blocked from signaling

107
Q

In _______ desensitization, signaling by both the stimulated receptor and by other teypes of receptors is attenuated

A

heterologous

108
Q

What receptors are blocked in heterologous desensitization

A

stimulated and unstimulated

109
Q

Why does heterologous desensitization occur?

A

covalent modification of receptors and other processes such as competion for shared second messenger

Pharm Block 1 (23 decks)

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