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The NF-kB pathway Flashcards

1
Q

which pathway alls the cell/organism to respond to environmental threats

A

NF-kB, p53 and HIF

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2
Q

what are the environmental changes that sets off the p53, NF-kB and HIF pathway

A

DNA damage, Infection, Hypoxia and physical stress

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3
Q

what pathway is set off by p53

A

DNA damage

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4
Q

what pathway is set off by NF-kB

A

Infection

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5
Q

what pathway is set off by HIF

A

Hypoxia

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6
Q

what are the cellular responses to these pathways

A

Gene expression, repair, programmed death and immune response

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7
Q

what is NF-kB

A

Nuclear factor of the kappa immunoglobulin light chain in B cells

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8
Q

what is the function Rel homology Domain (RHD)

A

encodes the DNA binding and dimerisation functions of NF-kB

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9
Q

what are the proteins proteolytically processed from the precursors p105 and p100

A

p50 and p52

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10
Q

T/F p105 is inducibly activated into p50

A

false it is generally constitutive where as p100 is inducible

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11
Q

NF-kB needs to _ to bind to DNA

A

dimerise

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12
Q

how can p100 and p105 function as a IkB-like inhibitor

A

contain ankyrin repeats in their C-termini

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13
Q

what are the non conserved transcriptional activation domain

A

TA1/TA2, TAD, SD1, SDII

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14
Q

what is a E3 ubiquitin ligase

A

a protein that facilitates the attachment of ubiquitin chains to a target protein

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15
Q

what is ubiquination

A

Ub is conjugated to proteins that are destined for degradation by an ATP-dependent process that involves three enzymes

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16
Q

how is a protein ubiquiniation started

A
  • a chain of 5 Ub molecules attached to the protein substrate is sufficient for the complex to be recognised by the 26S proteasome
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17
Q

when 26S proteasome attaches to the protein, what happens next

A

after ATP dependent reactions occurs, Ub is removed and the protein is linearised and injected into the central core of the proteasome where it is digested to peptide

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18
Q

what happens to digested proteins after degradation from Ub

A

The peptides are degraded to amino acids by peptidases in the cytoplasm or used in antigen presentation

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19
Q

NF-kB is induced by

A

Inflammatory cytokines,
Bacterial products,
Viral proteins & infection, DNA-damage, Cell Stress

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20
Q

NF-kB regulates

A

The immune and inflammatory responses, Stress responses, Cell survival and cell death, Cell adhesion, Proliferation

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21
Q

how are they induced and how do they regulate all these things

A

This is accomplished through the
regulation of 100’s (possibly 1000’s) of NF-
κB gene targets - but not all at the same
time, in the same way in all cell types

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22
Q

what are the specific stimuli which binds to the ligand receptors on the cell

A

ionising radiation, cytokines - inflammatory cytokines tumour necrosis factor a (TNFa) and interleukin 1 (IL-1), growth factors, bacterial lipopolysaccharide (LPS) and hypoxia

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23
Q

when not induced, what is NF-kB form in the cell

A

in-active cytoplasmic complex, bound to its inhibitor protein IkB

24
Q

upon cellular stimulation, IkB becomes _

A

phosphorylated which in most cases results in its ubiquinitnation and degradation from 26S proteasome.

25
where does NF-kB translocate to after freeing
nucleus
26
what are the 3 core subunits of the IkB (IKK) complex
IKKa and IKKB and the IKKy (NEMO)
27
what are the catalytic subunits and which is the regulatory subunit
IKKa and IKKB = catalytic NEMO = regulatory
28
both IKKa and IKKB have a _ domain with _
kinase, with an activation loop
29
NEMO contains CC1 and CC2 which stand for
coiled coil regions 1 and 2
30
what is the similarities between p105+p100 and IkB
they contain ankyrin repeat motifs in their C termini and PEST domain (rich proline, glutamate, serine and threonine)
31
what are the two NF-kB activation pathways
Canonical classical pathway and non-canonical (alternative) pathway
32
which p protein is associated which the classical and which is linked to the alternative
p50 is linked to the classical and p52 is linked to the alternative
33
how does the alternative pathway occur
NIK causes a dimer of IKKa to remove P100 Ankyrin repeats which causes p52 version of NF-kB to localise to the nucleus
34
NF-kB/IKK regulates many target genes associated both with normal responses to infection and stress as we as with human diseases (cancer, inflammation etc)
Inflammation, proliferation, survival, angiogenesis, Tumor promotion & metastasis, Cell death & anti-proliferative effects
35
What is a danger with NF-kB
when control is lost of them, they become nuclear - causing cancer, arthritis, AIDS, Asthma, Diabetes and atherosclerosis
36
interaction with proteins can be determined by _
orientation
37
how does diversity and dimerisation affect NF-kB function
- NF-kB family is multi-gene which when two proteins dimerise allows the formation of many different types with different properties/function
38
hows does NF-kB target different genes
different subunits have subtly different DNA binding specificity, however many NF-kB target genes are shared between subunits
39
When NF-kB translocates into nucleus, what can happen?
- Kinases, Acetylases and phosphatases can act on NF-kB - NF-kB can bind to DNA for either, transcriptional repression, activation as well as promoter targeting and selectivity
40
when NF-kB binds to DNA relating to transcription repression what binds to RelA-TAD subunit
Co-repressor
41
when NF-kB binds to DNA relating to transcription activation what binds to RelA-TAD subunit
Co-activator
42
when NF-kB binds to DNA relating to promoter targeting and selectivity, what binds to RelA-RHD
heterologous transcription factors and DNA binding proteins
43
How can chromatin be remodelled around NF-kB dependent genes
NF-kB can recruit chromatin remodellers or can rely on other proteins to do this -HATs and Swi/Snf
44
P65 =
RelA
45
what is a beta interferon
a and b interferon (IFN) are produced from viral infection as well as other subsets of genes
46
What does the expression of a and B interferon cause, as well as why does it need to be controlled
- a and B interferon bind specific cell surface receptors which results in a signalling cascade leading to the activation of over 50 anti-viral genes. - Needs to be controlled as viral response needs to be activated when infected, not in response to other immunological challenge
47
what happens if the individual txn factor binding sites in the B IFN enhancer was exploited and multimerised,
they can act as a viral inducible promoter, however they have varying basal levels of activity and can respond to other inducers
48
what allows the Beta-interferon enhancers to perform its function
- key is the combination and organisation of the enhancer -spacing and orientation allows appropriate protein:protein contact
49
The transcription factors binding the B IFN enhancer all interact to form the _
enhanceosome complex
50
This complex forms a I_ I_ which allows _
- interaction interface - allow the high affinity recruitment of transcriptional coactivators such as p300/CBP (these proteins can bind more than one transcription factor at one time
51
Individual transcription factor:coactivator interactions can be described as
generally weak
52
Instead of Individual transcription factor: coactivator interactions what is favoured
the formation of coactivator complexes only at the promoters and enhancers
53
what is created and what is required in coactivator complexes only at the promoter and enhancers
created = appropriate interaction interface required = coactivator activity
54
Which NF-kB complex works at the B IFN enhancer
p50/RelA(p65)
55
After chromatin remodelling NF-kB can directly induce transcription by helping to recruit what ?
Basal transcription machinery

CMB2001 (11 decks)

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