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BIO230 Section 2 > 2.9: Signaling via Protein Modifications > Flashcards

2.9: Signaling via Protein Modifications Flashcards

1
Q

state and describe the two mechanisms of signaling via enzyme coupled receptors

A
  1. phosphorylation: signal perception triggers activation of receptor kinases or receptor associated kinases
  2. proteolysis: signal perception triggers protein cleavage or degradation
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2
Q

state the 3 examples of phosphorylation

A
  1. receptor tyrosine kinases
  2. tyrosine kinase associated receptors
  3. receptor serine/threonine kinases
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3
Q

describe the common structure of receptor protein kinases (RTKs) and their functions

A
  • different ec domains bind different ligands
  • has tm domain
  • ic tyrosine kinase domain phosphorylate different targets at tyrosine residues
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4
Q

how are RTKs activated

A
  1. ligand binding (signal)
  2. transautophosphorylation
    (trans = on diff RTK molecule, auto = RTKs can act as RTK)
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5
Q

state the structure of activated RTKs

A

dimers

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6
Q

t/f after signal proteins bind to RTKs, the transautophosphorylation must activate each others kinase domains are the same time

A

true

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7
Q

t/f the signal protein for RTKs don’t always have to be dimers

A

yes

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8
Q

RTK transautophosphorylation can recruit other signaling molecules, this means the acitvated RTK can act as what type of protein

A

scaffold protein

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9
Q

when rtks act as a scaffold, what do proteins bind to

A

phosphorylated tyrosine

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10
Q

which domains can signaling proteins bind to RTKs to

A

SH2 or PTB domains

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11
Q

explain how signaling proteins can bind to RTKs via SH2 or PTB domains

A

each SH2 domain has two binding sites for specificity: recognizes the phosphorylated tyrosine, recognizes nearby amino acids
these ensure that SH2 domains bind to specific phosphorylated proteins

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12
Q

t/f activated RTKs can recruit other signaling molecules and often activates Ras-GEFs

A

true

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13
Q

Ras family proteins are related to other monomeric ________

A

GTPases

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14
Q

Many RTKs signal to activate _____ monomeric GTPases

A

Ras

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15
Q

what are MAP kinase

A

mitogen activated protein kinase - signal that generates mitosis

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16
Q

do all MAP kinases activate mitosis

A

no

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17
Q

which cascade can activated ras activate

A

MAP kinase cascades

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18
Q

what can MAP kinases convert a short term RTK activation at the cell surface into

A

a stable/long term change in gene expression

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19
Q

which type of feedback do MAP kinases provide

A

negative feedback

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20
Q

How many of each of the following do humans have: MAPKKK (Raf), MAPKK (Mek), MAPK (Erk)

A

MAPKKK: ~7
MAPKK: 7
MAPK: 12

21
Q

state what type of changes the effector proteins cause at the end of the MPA kinase cascade

A
  • changes in protein activity (protein x, protein y)
  • changes in gene expression (transcription reg prot A and B)
22
Q

state what can provide specificity to MAP kinase cascades

A

scaffold proteins

23
Q

drosophila sevenless signaling is an example of what

A

RTK signaling

24
Q

Drosophila compound eyes are made of ___________
Each ommatidia has _ photoreceptor cells (R1-R_)
The R_ cells is required to detect UV light

A

ommatidia, 8, 7

25
Q

which is the first cell to differentiate in the ommatidia (R what) and which is last

A

R8, R7

26
Q

in sevenless signaling:
RTK = _________
Ligand = _________
Adaptor protein = _________
Ras-GEF = _________

A

RTK = Sevenless (Sev)
* Ligand = Bride of Sevenless (Boss)
* Adaptor protein = Grb2 (Drk)
* Ras-GEF = Son of Sevenless (Sos)

27
Q

what is the end product of the sevenless signaling pathway

A

differentiation into R7

28
Q

describe how RTKs can signal through phosphoinositides (PIPs)

A
  1. RTK activated
    by a survival
    factor
  2. RTK activates
    PI 3-kinase
  3. PI 3-kinase converts PI(4,5)P2 to
    PI(3,4,5)P3
  4. PDK1 & Akt bind PI(3,4,5)P3
  5. PDK & mTORC2 phosphorylate Akt
  6. Akt phosphorylates Bad to release
    Bcl2 to inhibit apoptosis
    (in order to survive = can’t die)
29
Q

there can be cross talk between ?

A

RTK and GPCR signaling

30
Q

what type of receptors have no kinase activity

A

cytokine receptors (no tyrosine kinase domain)

31
Q

those receptors that have no kinase activity, they associate with what to be able to signal

A

cytoplasmic tyrosine kinase

32
Q

which mechanisms remain similar between tyrosine kinase associated receptors and RTKs

A

transautophosphorylation and protein binding to the phosphorylated receptor

33
Q

compare and contrast between receptor serine/threonine kinases and RTKs

A

Similar to RTKs:
* Extracellular ligand binding
domain
* Transmembrane domain
* Intracellular kinase domain
* Multiple receptors associate
in response to signals
But: kinase domains
phosphorylate serine and/or
threonine residues in targets

34
Q

delta notch is an example of what type of signaling and notch signaling involves signaling via (2)

A
  • contact dependent signaling
    1. endocytosis
    2. proteolysis
35
Q
  1. where in the cell are notch proteins made and why
  2. where is notch cleaved into two pieces
A
  1. in the ER bc TM
  2. golgi
36
Q

state the signifier of proper notch

A

the cleavage

37
Q

do the cleaved pieces of notch stay together or go apart when they move to the plasma membrane

A

stay together

38
Q

interaction with delta results in further/less notch proteolysis

A

further

39
Q

the ______ part of notch directly interacts with delta on the surface of the other cell, delta notch is _______ into the delta expressing cell for proper gene expression and the remainder of notch is cleaved at ____ more sites

A

extracellular, endocytosed, two

40
Q

after delta-notch is endocytosed into the delta expressing cell, the remainder of notch is cleaved at how many more sites

A

two

41
Q

does the cytosolic head or tail of notch move to the nucleus and what does it promote

A

tail, the notch tail promotes transcription of notch target genes

42
Q

if there is transcription of notch target genes, is delta activated or repressed in this cell

A

repressed - but you might have some if the proteins made were repressors

43
Q

does the cell with active notch target genes differentiate or not differentiate

A

not differentiate

44
Q

how do notch small fragments free up in the ec space

A

through cleavage

45
Q

state the 4 types of mechanisms that hedgehog signaling combines

A
  1. GPCRs, cAMP, PKA
  2. proteolysis
  3. cytoskeleton - mediated transport
  4. paracrine signaling
46
Q

describe the actions when hedgehog signaling is present

A
  1. Hedgehog binds and inactivates Patched
  2. Smoothened is active and moves to the tip of the primary cilium
  3. Gpr161 and PKA are inactive
  4. Gil3 is not proteolytically processed so it
    does not inhibit hedgehog target genes
  5. SuFu and Gli2 move along microtubules to
    the tip of the primary cilium
  6. Smoothened releases Gli2 from SuFu
  7. Gli2 moves along microtubules from primary cilium to nucleus
  8. Gli2 activates hedgehog target genes
47
Q

describe the sequence of events when there is no hedgehog signal

A
  1. Patched is active in the cilium
  2. Active Patched inhibits Smoothened and
    keeps Smoothened out of the primary cilium
  3. SuFu binds and inhibits Gli2 & Gli3
  4. GPCR (Gpr161) is active
  5. Active Gpr161 promotes cAMP synthesis
  6. cAMP activates PKA
  7. PKA phosphorylates Gli3
  8. Gli3 phosphorylation causes Gli3 proteolytic processing
  9. The remaining fragment of Gli3 moves to the nucleus to repress expression of hedgehog target genes
48
Q

what processes are the following involved in
1. notch (3)
2. hedgehog (Shh) (5)

A
  1. tissue patterning, neurogenesis, stem cell renewal
  2. neural tube closure, tissue patterning, limb development, lung development, stem cell renewal
49
Q

Which of the following terms best describes Sevenless signaling?
a) Contact dependent signaling
b) Paracrine signaling
c) Two-component signaling
d) Receptor threonine/serine kinase signaling

A

A

BIO230 Section 2 (12 decks)

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