lecture 24 redone Flashcards

1
Q

PH domain
proteins with PH domain bind to

A

phosphorylated inositol phospholipis in the plasma membrane (localises signallng)

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2
Q

PTB domain

A

binds phosphotyrosine (P-Y) residues

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3
Q

SH2 domain
2 domain binds phosphotyrosine residues surrounded by unique proetin sequences

A
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4
Q

SH3 binds to specfically to proline rich regions

A
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5
Q

insulin receptor is a tetrameric tyrosine kinase receptor

A

2alpha , 2 beta , alpha at top so binds

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6
Q

the IR is expressed as two isoforns

A

isoforn A and B

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7
Q

beta subunit has tyrosin kinase redisues meaning it can

A

phosphorylate tyrosine when activated

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8
Q

Shc - SH2 containing apapter protein
Shc has PTB and SH2 domain
shc can bind to insulin receptor, when they bind tyrosine is phosphorylates uncoveing a binding site for binding SH3 domain

A

e.g Grb2 from SH3 domain binds to Shc

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9
Q

IRS = insulin receptor substrate (adapter protein)
IRS1,2,3,4 contains a

A

PH and PTB domain

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10
Q

PH and PTB domain enable binding to phosphorylates insulin receptor, after binding the IRS becomes phosphorylated on tyrosines by

A

IR tyrosine kinase activtity

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11
Q

IRS has wq potential tyrosine phosphorylation sites

A

making it a dokcing protein for proteins with SH2 domains

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12
Q

PI3 kinase, Grb2 and SHP2

A

can bind to IRS as the have SH2 domains

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13
Q

insulin receptor is bound to by IRS which is bound to by Shc via the Grb2, interacts with

A

SOS when bound

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14
Q

SOS acts as a GDP/GTP exchange factor
ras ia inactive when bound to GDP ras is activtated when its exchanged for GTP. Ras GTP activates

A

raf

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15
Q

raf activtes

A

MAPKK

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16
Q

MAPKK activates

A

MAP- kinase whcih drives growth, differentition adn proliferation

17
Q

PI3 can bind to IRS via SH2 domain, this leads to generation of

A

PIP3

18
Q

PIP3 is a binding parter for proteins with PH domains eg

A

AKT

19
Q

PI3K adds a phosphorylates PIP3

A

PDK1 binds to PIP3 and it enables the phosphorylation of a redisue on AKT

20
Q

mTORC2 phosphorylates AKT

A

dual phosphorylation activates AKT

21
Q

when AKT is phosphorylated it can phosphorylate other proteins
AS160 blocks movement of vesicles containing GLUT4 by

A

regulating Rab

22
Q

for Ran to facilitate the movement to the membrane it needs to be bound to

A

GTP when AS160 prevents them binding

23
Q

phosphorylation of AKT leads to phosphorylation of

A

AS160 leading to its inactivation causing GLUT4 to translocate

24
Q

AKT phosphorylates TSC2 which regulates

A

mTORC1

25
Q

activation of mTORC1 activates elF4E-BP1 and S6K1 leads to translation initiation adn ribosome biogensis

A

protein synthesis ^

26
Q

FOXO1 induces G6PC and PEPCK (enzymes of gluconeogenesis) and FOXO1 represses GCK (glucokinase) AKT phosphorylates FOXO1 which then translocates to the cytoplasm wheres its

A

ubiquitinated and degreaded allowing repression og G6PC and PEPCK and insuction og glucokinase

27
Q

glycogen sythase kinase 3 (GSK3) is inactivates when phosphorylated by AKT, GSK when is activate is able to phosphorylate many proteins

A

GSK phosphorylaltes glycogen synthase making it inactive and not mych glycogen is formed
AKT phosphorylates GSK3 making it inactive promoting glycogen Nand protein synthsis