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Dynamic Cell > TKR 2 - cell survival > Flashcards

TKR 2 - cell survival Flashcards

1
Q

alternative mechanisms of TKR

A

EGFR
- EGF binds to EGFR
= conformational change that allows association of 2 activated receptors

INSR

  • homodimeric structure where intracellular domain held apart
  • insulin binding induces conformational change
  • > brings kinase domains together
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2
Q

RTK activation of SH2/SH3 domain proteins by…?

A

PI 3-kinase
-> cell survival pathway

Ras-MAP-kinase
-> cell proliferation pathway

Phospholipase C

  • > activates IP3 pathway
  • cross-talk with GPCR signalling
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3
Q

adaptor proteins

- what are they?

A

contain no catalytic domains

serve as link between receptor + intracellular signalling proteins e.g. GNRP/GEF

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4
Q

GNRP/GEF

  • what are they?
  • does what?
A

guanine nucleotide releasing protein

Ras-guanine nucleotide exchange factor

activates Ras monomeric GTPase

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5
Q

Ras superfamily

A

small monomeric GTPase

(unlike trimeric GTPases in GPCR signalling)

relay RTK signals
-> cell proliferation

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6
Q

GNRP/Ras-GEF activates Ras

- process

A

recruitment of Grb2 and Ras-GEF to activated receptor
-> brings them into proximity with Ras molecules

interaction of Ras-GEF with Ras
-> conformational change of Ras
-> releases GDP
-> acquires GTP 
-> conformation change
= activate Ras

-> downstream signals leads to proliferation

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7
Q

what 2 factors are key to GNRP/Ras-GEF activating Ras?

A

signal protein localisation

conformational change

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8
Q

Ras molecular switch

A

GEF/GNRP
-> promotes GDP release
= activates Ras

GAPs promote Ras GTPase activity
-> inactivates Ras via GTP hydrolysis

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9
Q

activated RTK promotes transient Ras activation

A

indirect association of GEF with RTK via Grb2
-> rapid activation of Ras

some GAPs associate directly with RTKs

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10
Q

why is Ras self-inactivating?

A

has intrinsic GTPase activity

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11
Q

how is RTK phosphorylation reversed?

A

by tyrosine-specific protein phosphatases

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12
Q

Ras activates a cascade of serine/threonine-kinases

A

via phosphorylating Raf

  • > phosphorylates Mek
  • > phosphorylates Erk
  • > produces proteins or regulatory proteins

-> change protein activity or gene expression

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13
Q

Ras-MAPK pathway

- discovery

A

in Drosophila genetic experiments

based on inability of mutant flies to detect UV light

  • > screen offspring
  • > looking for genes that regulate eye development
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14
Q

drosophila eye development

A

R8

  • > R5 + R2
  • > R4 + R3
  • > R6 + R1
  • > R7

R7 specialised to detect UV light

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15
Q

Sevenless mutants

A

lack R7 cell

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16
Q

Sevenless

- molecule type

A

an RTK

17
Q

Sev

  • ligand
  • Ras-GEF
  • receptor kinase
A

Boss

Sos

Drk

18
Q

Boss and Sev

A

anchored to PMs

  • can only ‘talk’ to adjacent cells
    i. e. R8, R6 + R1 cells with R7 cell
19
Q

Boss-Sev pathway in R7 cells

A
  1. boss binds to Sev RTK = activated
  2. Drk binds to phosphate on Sev
  3. Drk binds to Sos
  4. Sos releases GDP from Ras
  5. GTP binds to Ras
  6. Activated Ras sends downstream signals
    (proliferation)
20
Q

PI-3 kinase

- what do they do?

A

forms products with P groups at 3rd position of 6-carbon inositol ring of PI
(phosphatidylinositol)

= forms PIP

21
Q

PI-3 kinases promote cell survival

- proteins recruited

A

PI-3 is rapidly recruited to active RTK

PDK1 + PKB are recruited to membrane via interactions with their PH domains + IP products of PI3-kinase

22
Q

PI-3 kinases promote cell survival

- process to BAD phosphorylation

A

proteins brought into close proximity

  • > PDK1 activated by PIP
  • > phosphorylates PKB
  • > PKB conformation change + dissociates from PIP3
  • > PKB phosphorylates target protein = BAD
23
Q

PI-3 kinases promote cell survival

- post BAD-phosphorylation

A

BAD normally associated with death inhibitory protein

phosphorylated BAD
-> conformation change
-> releases death inhibitory protein
= prevents apoptosis

= cell survival

24
Q

3 types of molecular activation

  • what are they?
  • what do they all result in?
A

phosphorylation

GDP to GTP exchange

protein-protein interaction

–> conformation change

25
Q

what factor is also important to conformation change?

A

signal molecule localisation

Dynamic Cell (15 decks)

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