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

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
RAS inactivate by
RasGAP
26
Ras extra mutation can lead to
cancer
27
different members of MAP kinase family can elicit different cellular pathways via
having different MAPKKK/MAPKK/MAPK activate
28
how many different MAP family we have
14 MAPKKK 7 mAPKK 13MAPK
29
In signal transduction, linear pathway does not happen instead there is
conergence/divegence
30
Nuclear Receptors
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
Nuclear receptors have two main domain
1- LIganid binding domain 2- DNA binding domain
32
steroid receptors act by binding
HRE (hormone response element)
33
Binding to HRE can be
enhanced or repressed gene expression
34
DNA binding doamin is
two zinc-finger motifs
35
starting material for synthesis steroid hormines
cholesterool
36
cortisol is
glucocorticoids
37
aldesterone is
mineralcorticoids
38
corstisol pathway
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
Ligand gated channels
channel scan be opened/closed by binding of a ligand allow passage of specific ions ligand can be neurotransmitters
40
Ligand gated activation
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**