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CMB2001 > The NF-kB pathway > Flashcards

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
Q

where does NF-kB translocate to after freeing

A

nucleus

26
Q

what are the 3 core subunits of the IkB (IKK) complex

A

IKKa and IKKB and the IKKy (NEMO)

27
Q

what are the catalytic subunits and which is the regulatory subunit

A

IKKa and IKKB = catalytic
NEMO = regulatory

28
Q

both IKKa and IKKB have a _ domain with _

A

kinase, with an activation loop

29
Q

NEMO contains CC1 and CC2 which stand for

A

coiled coil regions 1 and 2

30
Q

what is the similarities between p105+p100 and IkB

A

they contain ankyrin repeat motifs in their C termini and PEST domain (rich proline, glutamate, serine and threonine)

31
Q

what are the two NF-kB activation pathways

A

Canonical classical pathway and non-canonical (alternative) pathway

32
Q

which p protein is associated which the classical and which is linked to the alternative

A

p50 is linked to the classical and p52 is linked to the alternative

33
Q

how does the alternative pathway occur

A

NIK causes a dimer of IKKa to remove P100 Ankyrin repeats which causes p52 version of NF-kB to localise to the nucleus

34
Q

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)

A

Inflammation, proliferation, survival, angiogenesis, Tumor promotion & metastasis, Cell death & anti-proliferative effects

35
Q

What is a danger with NF-kB

A

when control is lost of them, they become nuclear - causing cancer, arthritis, AIDS, Asthma, Diabetes and atherosclerosis

36
Q

interaction with proteins can be determined by _

A

orientation

37
Q

how does diversity and dimerisation affect NF-kB function

A
  • NF-kB family is multi-gene which when two proteins dimerise allows the formation of many different types with different properties/function
38
Q

hows does NF-kB target different genes

A

different subunits have subtly different DNA binding specificity, however many NF-kB target genes are shared between subunits

39
Q

When NF-kB translocates into nucleus, what can happen?

A
  • 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
Q

when NF-kB binds to DNA relating to transcription repression what binds to RelA-TAD subunit

A

Co-repressor

41
Q

when NF-kB binds to DNA relating to transcription activation what binds to RelA-TAD subunit

A

Co-activator

42
Q

when NF-kB binds to DNA relating to promoter targeting and selectivity, what binds to RelA-RHD

A

heterologous transcription factors and DNA binding proteins

43
Q

How can chromatin be remodelled around NF-kB dependent genes

A

NF-kB can recruit chromatin remodellers
or can rely on other proteins to do this
-HATs and Swi/Snf

44
Q

P65 =

A

RelA

45
Q

what is a beta interferon

A

a and b interferon (IFN) are produced from viral infection as well as other subsets of genes

46
Q

What does the expression of a and B interferon cause, as well as why does it need to be controlled

A
  • 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
Q

what happens if the individual txn factor binding sites in the B IFN enhancer was exploited and multimerised,

A

they can act as a viral inducible promoter, however they have varying basal levels of activity and can respond to other inducers

48
Q

what allows the Beta-interferon enhancers to perform its function

A
  • key is the combination and organisation of the enhancer
    -spacing and orientation allows appropriate protein:protein contact
49
Q

The transcription factors binding the B IFN enhancer all interact to form the _

A

enhanceosome complex

50
Q

This complex forms a I_ I_ which allows _

A
  • 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
Q

Individual transcription factor:coactivator interactions can be described as

A

generally weak

52
Q

Instead of Individual
transcription factor: coactivator interactions what is favoured

A

the formation of coactivator complexes only at the promoters and enhancers

53
Q

what is created and what is required in coactivator complexes only at the promoter and enhancers

A

created = appropriate interaction interface
required = coactivator activity

54
Q

Which NF-kB complex works at the B IFN enhancer

A

p50/RelA(p65)

55
Q

After chromatin remodelling NF-kB can directly induce transcription by helping to recruit what ?

A

Basal transcription machinery

CMB2001 (11 decks)

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