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Control Of Gene Expression > Nf Kb Pathway > Flashcards

Nf Kb Pathway Flashcards

1
Q

What types of things does NF kb respond to

A

Infection Eg via cytokines or bacterial products
Viral proteins
Dna damage
Stress

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2
Q

Give an example of a sensor Eg for the cytokines

A

TLReceptors which cause signalling pathway

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3
Q

Nf kb is a family of tf. Name the types

A

Rel A (p65)
Rel B
C rel

Nfkb 1 (P105) —-> p50
Nfkb 2 (P100)—-> p52
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4
Q

What domain is present in all nfkb and what does it do

A

RHD

Rel homology domain - encodes the dna binding site and the dimerisation functions

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5
Q

What are on p105 and p100 which allows them to act as Ikb inhibitors

A

Ankyrin repeats (lost when they convert to p50 and p52)

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6
Q

How are p105 and p100 converted

A

Proteolytically processed

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7
Q

What is the trans activation domain on rel A p65 called

A

TA 1 and 2

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8
Q

What is the transactivation domain called on rel B and c rel

A

Rel B - TAD

C rel- sd1 and sd2

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9
Q

How are ta1/2, tad and sd 1/2 different

A

They will activate and regulate differently (not homologous)

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10
Q

When was nfkb first found in evolution

A

I’m multicellular organisms ie not yeast or bacteria

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11
Q

Which enzymes causes ubiquitin chains to be added to proteins which are then degraded by the proteasome

A

E3 ubiquitin ligase

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12
Q

What does proteasome use to degrade proteins in ubiquitination

A

Atp hydrolysis

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13
Q

What is the pathway called which activates nfkb

A

Canonical pathway

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14
Q

Why is nfkb rapidly activated

A

Because it is already made in the cytoplasm but stays as an inactive complex

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15
Q

Which dimer is the most common of nfkb

A

P50 and rel A

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16
Q

What are the 3 different types of IkB inhibitor

A

Ikb a
Ikb b
Ikb e

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17
Q

Which parts of Ikb inhibitors can bind and inactivate nfkb in cytosol

A

Ankyrin repeats

18
Q

Which 2 ways does Ikb binding via ankyrin repeats inactive nfkb

A

Conformational change in it so can’t bind to dna

Hides the nuclear localisation sequence of nfkb

19
Q

How is ikb degraded

A

Phosphorylation and ubiquitination at its conserved sites

20
Q

What complex which inactivates Ikb get stimulated when w signal to switch nfkb is sensed Eg tnf a

A

Ikb kinase (IKK) complex

21
Q

What are the 3 ikk Ikb kinases

A

IKK a
IKK b
Nemo IKK y

22
Q

What 3 things make up IKK a and b

A

Kinase domain
Dna binding Eg LZ,zf,hlh
Nemo binding domain NBD

23
Q

What do IKK a and IKK b do

A

Phosphorylate and therefore cause ubiquitination of Ikb inhibitor

24
Q

How is the IKK complex made

A

1 IKK y will bind with the IKK a and ikk b nemo binding domains

25
Q

What is cc1 and cc2 on nemo IKK y

A

Coil coil domains

26
Q

Name a few things nfkb does when active

A

Inflammation via releasing cytokines

Cell survival genes

Cell apoptosis inducing genes

Metastasis/cell adhesion inducing genes

Angiogenesis

Proliferation

27
Q

How does nfkb activation and production cause a feedback loop which is why nfkb is regulated via Ikb

A

Activated by cytokines and releases cytokines itself

Causes constant nuclear action causing things like proliferation and inflammation

28
Q

Why are dimers like rel a p50 important

A

They bind at a specific orientation on genes to regulate them

29
Q

Once nfkb is activated via degradation of Ikb what happens in nucleus

A

Nfkb are modified Eg via phosphorylation,acetylation,de phosphorylation

30
Q

What does modification of nfkb cause

A

Either binding of co repressors or co activators
Or
Binding of other tf which work cooperatively or antagonistically

31
Q

What does nfkb need to get access to promoters/enhancers

A

Chromatin remodellers Eg swi2/snf2

32
Q

How are chromatin remodellers brought to allow nfkb action

A

By nfkb itself or by other proteins like HATs which attract swi/snf2 via bromodomain

33
Q

What type of co activators does rel A via modification (phosphorylation) attract to allow its access to promoters

A

Cbp/p300

Has HAT activity and recruits of TFs

34
Q

Why does nfkb get activated in viral infections

A

Viral rna activates nfkb

35
Q

Which genes are usually up regulated for antiviral/ infection response

A

Ifn b and cytokines

36
Q

Why does Sars cov cause inflammation by disrupting nfkb

A

Nfkb can’t upregualte the ifn gene which is antiviral.

Only cytokines released

37
Q

Which TFs work with nfkb rel a and p50 to activate enhancer for ifn b gene

A

C jun, atf 2, irfs

38
Q

What is important in the tf recruitment on the ifn b enhancer

A

Needs to be right spacing and orientation of the c jun, atf 2 and irs and rel a/p50

39
Q

What is the binding of all tf on the ifn b called

A

Enhancesome complex

40
Q

What does the enhancesome complex do

A

Allows co activators like p300/cbp which are HATs to be attracted

They allow better pic recruitment and recruit remodellers like swi2/snf2

Control Of Gene Expression (13 decks)

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