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BMS2002 > L17 > Flashcards

L17 Flashcards

1
Q

what are the types of NF-kB signaling pathways

A

canonical (classical)

Non-canonical (alternative)

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2
Q

describe the canonical pathway of NF-kB signaling

A

receptor is triggered by TNFRs, TLRs, and other stress signals

activated receptor interacts with the IKK complex (IKK alpha, IKK beta, and IKK gamma)

only active catalytical kinase is IKK beta

IkBa keeps transcription factor dimer (p50 and p65) inactive

IKK beta phosphorylates IkBa triggering its ubiquitination

IkBa is degraded by proteosome and transcription factor is activated

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3
Q

what are the catalytical subunits of the IKK complex

A

IKK alpha and beta

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4
Q

what is the regulatory subunit of the IKK complex

A

IKK gamma

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5
Q

describe what happens in the non-canonical pathway of NF-kB

A

receptor is triggered by LTbetaR and BAFF-R

NIK is activated which phosphorylate IKK alpha

IKK alpha phosphorylates p100 that is binding to RelB

p100 is processed to p52 and p52 binds to RelB

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6
Q

which IKK subunit is active in the non canonical pathway

A

IKK alpha

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7
Q

what is RelA

A

p65

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8
Q

what does The Rel Homology Domain (RHD) do

A

encodes the DNA binding and dimerisation functions of NF-kB

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9
Q

which protein produces p50

A

p105

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10
Q

which protein produces p52

A

p100

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11
Q

what is special about p100 and p105

A

they contain ankyrin repeats in their C-termini that allow them to function as IkB inhibitors

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12
Q

what are the non conserved transcriptional activation domains in NF-kB proteins

A

TA1/TA2, TAD, SD1, SDII

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13
Q

NF-kB contributes in cancer markers

A

True

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14
Q

Tumors that Express Aberrantly Active NF-κB/Have Altered NF-κB/IκB proteins

A

True

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15
Q

why cant we inhibit NF-kB

A

causes irregulation of the NF-kB

interrupts activation of the immune system, apoptosis, and homeostasis.

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16
Q

check slide 16 for extra reading

A

CHECK IT FOR THE ESSAY

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17
Q

which proteins have regulatory functions in NF-kB signaling

A

IKB-alpha

IKK-gamma (NEMO)

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18
Q

p53 is activated by similar triggers as NF-kB

A

true

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19
Q

how is p53 different to NF-kB

A

p53 triggers cell death if damage can not be repaired (promotes tumor suppression)

NF-kB promotes cell survival (promotes tumor promoting)

20
Q

describe the p53 signaling pathway

A

p53 is kept inactive by MDM2 or its isoform MDMX. these proteins ubiquitinate p53 leading to its degradation by proteosomes

stress conditions activate ATM and ATR which modify p53 structure

p53 separates from MDM2 and MDM2 is degraded

p53 regulates genes in the nucleus

21
Q

what genes does p53 regulate

A

p21

BAX

GADD45/PCNA

22
Q

what does p21 do

A

produced by p53

acts on ciclin and CDK complexes

also acts on pRB and E2F pathways

leads to cell cycle arrest (G1/S)

23
Q

what does BAX do

A

triggers apoptosis

24
Q

what do GADD45/PCNA do

A

promote DNA repair

25
Q

what are the domains of the p53 protein

A

N-terminal domain

The core domain

The c-terminal domain

26
Q

describe the N-terminal domain

A

residues (1-99)

contain a sub-transactivation domain and a proline rich domain which may be involved in regulation of apoptosis

27
Q

describe the core domain

A

residues (100-300)

bind to specific DNA sequences

28
Q

describe the c-terminal domain

A

residues (323-393)

domain contains the tetramerization domain and another DNA binding site within the regulatory region

associated with ssDNA, insertion, deletion DNA mismatches or damaged DNA

29
Q

p53 forms tetramers

A

True

30
Q

what happens in cancer regarding NF-kB and p53

A

NF-kB antagonizes the functions of p53

31
Q

how does canonical NF-kB signaling lead to RA in dendritic cells

A

canonical NF-kB signaling drives the production of IL-15 and IL-18 allowing for further recruitment of dendritic cells

32
Q

how does non canonical NF-kB signaling lead to RA in dendritic cells

A

it produces IL-12, IL-17, IL-23, and IL-27 which activate T cells

33
Q

how does NF-kB pathway affect RA

A

C-Rel and NIK drive differentiation in Th-1 cells. Th-1 cells produce INF-gamma causing inflammation

C-Rel, Rel-A, and NIK differentiate Th-17 cells. Th-17 cells produce IL-17 which causes inflammation

34
Q

how does the non canonical pathway in B cells affect RA

A

NIK and IKK alpha activate the B cells

35
Q

what are the steps of activating the B cells that driven by NF-kB

A

germinal center formation

B cell proliferation

auto-antibody production

36
Q

how does NF-kB affect T reg cells in RA

A

increased TNF-alpha expression in RA symptoms increases NF-kB activity

Foxp3 is transcription factor that causes development of T reg cells

RelA and C-Rel positively regulate Foxp3 promoting T reg formation

NIK downregulates Foxp3 and impairs T reg responses

effect is debatable

37
Q

how does NF-kB activation affect Fibroblasts-like Synoviocytes (FLS)

A

decreases FLS apoptosis

proliferates FLS

causes ECM destruction

maintains chronic inflammation, angiogenesis, migration and invasion.

38
Q

how does NF-kB activation cause FLS proliferation

A

p50 and Rel A drive the production of CycD1

over proliferation causes hyperplasia and pannus formation

39
Q

what causes decreased FLS apoptosis

A

NF-kB activation releases cytokines which express antiapoptotic genes

it can also phosphorylate Ser 536 which inhibits p53

40
Q

what causes destruction of ECM by NF-kB pathway

A

IKK epsilon activates MMP1, MMP3, and MMP9 causing destruction of ECM

RelA causes the production of RANKL which causes ECM destruction

41
Q

how does p53 can control the homeostasis of DCs immune cells

A

down regulation of p53 in DCs leads to hyperactivation of NF-kB and MAPK pathway

this leads to enhance antigen presentation, maturation and activation of DCs

42
Q

less p53 means less CD4 T cells differentiation

A

True

43
Q

what does the lack of p53 do to T cells

A

more production of Th17, increasing IL-17

Wip-1 is reduce resulting in impaired development, increasing DNT cells

reduced FOXP3. Treg cells are reduced

44
Q

what does down regulation of p53 do to MQ

A

increase in M1 aggressive macrophages compared to M2

45
Q

p53 suppresses angiogenesis

A

True

46
Q

what does defective p53 do in RA-FLS

A

promotes apoptosis resistance and hyper-proliferation.

more direct activation of NF-kB leads to more activation

reduced MiR-22 production increases Cyr-61 activity. Cyr-61 produces more IL-6 driving the activation of NF-kB

defective p53 produces more VEGF which promotes angiogenesis

47
Q

MiR-22 regulates which protein

A

Cyr-61

BMS2002 (21 decks)

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