Signal Transduction 3 Flashcards

1
Q

receptors basic categories

A

1-Ligand gated channels
2-Plasma membrane receptors
—-linked to g proteins
—-linked to protein kinase
3-Nuclear protein

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2
Q

linked to protein kinase (plasma membrane)

A

RTK–Receptor Tyrosine Kinases

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3
Q

GPCR regulate

A

Shorter term metabolic changes

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4
Q

RTK regulate

A

differentiation, cell division, survival

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5
Q

signal that stimulate dividing cells is

A

growth factor

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6
Q

many growth factor share a common theme

A

1-growth factor binding result in dimerization of receptors
2-trans-auto-phosphorylate of cytoplasmic domain does not phosphorylate itself, phosphorylate the neighbor
3-cytoplasmic signalling activated by binding to phosphorylated tyrosine

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7
Q

cytoplasimic signalling molecules associate with receptors by

A

SH2 and PTB domains

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8
Q

SH2

A

amino acids chains contain binding pocket that interact with pTyr

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9
Q

Adaptors

A

act as linkers enabling
contain SH2/PTB domain
Additional protein-protein interaction

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10
Q

Adaptors with SH2 domain

A

GRB2 bind to RTK
SH3 domain associated with Sos

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11
Q

Adaptor with PTB domain

A

IRS bind with RTK
lead to phosphorylation of IRS tyrosine
pTyr act as scaffolding for SH@ enzymes

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12
Q

Effectors

A

1- STAT family
2- Signalling enzymes with SH2 Domains wich can directly bind to RTK

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13
Q

STAT family

A

SH2 domain STAT bind to RTK, phosphrylate tyrosine in STAT, allow STAT dmierize, forming functional tanscription factor, trnaslocate to nucleus

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14
Q

signalling enzyme (with Sh2 doamin and ability to bind with RTK

A

protein kinases
shp2
plc
GAPs

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15
Q

signalling enzyme mechanism

A

1- recruitment of enzyme
2-binding of pTyr can result in conformational changes in catalytic domain
3- phosphorylation of enzyme can increase/decrease catalytic activity

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16
Q

Termination

A

RTK doesn’t require Arrestin (GPCR need arrestin)
they have short motif interacting with AP2

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17
Q

After binding with AP2: (3outcomes)

A

1- can resume within endosome
2- traficked by lysosome for degradation
3- returned to cell surface RE-sensitization

18
Q

G protein act as —- and —- to regulate cellular events

A

switches and timers

19
Q

Ras

A

small monomeric G protein s

20
Q

accessory protein help switch ras on/off

A

GAP: GTP hydrolysis
GDI: inhibitor–GDP can’t reactivate
GEF: activate GDP to GTP

21
Q

activated G protein is —- based

A

time

22
Q

RAs-MAP

A

1-EGF to RTK extracellular domain
2-dimerize
3- trans auto phosphorylate
4- GRB2 high affinity for pTyr
5-GRB2 assocaite with Sos
6-Sos is RasGEF
7- binding GRB2 to pTyr, brings Sos near Ras, allowing GDP to be replaced by GTP
8- Ras-GTP has high affinity for MAPKKK
9- MAPKKK phosphrylate Serine and Threonine in MAPKK
10- MAPKK phosphorylate MAPK
11- Activated MAPK can phosphorylate over 160 proteins
12- Activate genes in cell proliferation

23
Q

multiple pathways can be activated at the same time

A

Diverngence

24
Q

RAS when in active state should be inactivate to —-

A

avoid constitutional stimulation

25
Q

RAS inactivate by

A

RasGAP

26
Q

Ras extra mutation can lead to

A

cancer

27
Q

different members of MAP kinase family can elicit different cellular pathways via

A

having different MAPKKK/MAPKK/MAPK activate

28
Q

how many different MAP family we have

A

14 MAPKKK
7 mAPKK
13MAPK

29
Q

In signal transduction, linear pathway does not happen instead there is

A

conergence/divegence

30
Q

Nuclear Receptors

A

Soluble protein that mediate action of steroid hormones
–lipid signaling molecule which can pass easily through plasma membrane
—-receptor itself is an effector(no cascade)

31
Q

Nuclear receptors have two main domain

A

1- LIganid binding domain
2- DNA binding domain

32
Q

steroid receptors act by binding

A

HRE (hormone response element)

33
Q

Binding to HRE can be

A

enhanced or repressed gene expression

34
Q

DNA binding doamin is

A

two zinc-finger motifs

35
Q

starting material for synthesis steroid hormines

A

cholesterool

36
Q

cortisol is

A

glucocorticoids

37
Q

aldesterone is

A

mineralcorticoids

38
Q

corstisol pathway

A

1- enter the target cell
2- bind to glucocorticoid receptor
3-receptor changes conformation of the protein
4-expose nuclear localization signal
5- enter nucleus
6- activate/inhibit transcription

39
Q

Ligand gated channels

A

channel scan be opened/closed by binding of a ligand
allow passage of specific ions
ligand can be neurotransmitters

40
Q

Ligand gated activation

A

1-AP moves down a neuron to NMJ
2-AP opens voltage-gated Ca channels
3- elevated Ca conc. triggers ACh exocytosis
4-ACh will open ligand-gated Na channels
5- Na flows in
6- AP moves along membrane into t-tubules
7- AP activate voltage-gated CA channels on SR
8- Ca is released into cytoplasm and act as second messenger
9-Troponin C undergo conformational change
10- relieving tropomyosin blockage of actin-myosin binding site
11- myosin can now cause interaction
calcium-induced-clacium-released