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cell proliferation > anti-inflammatory Nrf2 > Flashcards

anti-inflammatory Nrf2 Flashcards

1
Q

what is Nrf2 the interface of

A

redox homeostasis and intermediary metabolism

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2
Q

what are the main sections of glucose homeostasis

A

glutathione and thioredoxin biosynthesis and utilization and NADPH regeneration and utilization

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3
Q

what are the main sections of intermediary metabolism

A

carbohydrate metabolism, lipid metabolism, AA metabolism and penyose phosphate pathway/nucleotide metabolism

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4
Q

where does Keap1 bind to

A

the N-terminal domain on Nrf2

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5
Q

what does Keap1 do

A

represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

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6
Q

what does Keap1 catalyse

A

ubiquitination of Nrf2

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7
Q

what do electrophilic inducers do

A

disrupt the Keap1 cycle by modifying sensor cysteines of Keap1, preventing Nrf2 ubiquitination and Keap1 regeneration

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8
Q

what happens to Keap1 when electrophilic inducers are active

A

they accumulate and translocate to the nucleus

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9
Q

what is the cysteine-based sensor Keap1

A

a dimer of Keap1

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10
Q

how does EGFP-Keap1 degenerate

A

very efficiently

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11
Q

how does Nrf2-mCherry degenerate

A

not so efficiently

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12
Q

what is sulforaphane

A

an inducer of Nrf2

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13
Q

where does sulforaphane work on Nrf2

A

it reacts with cysteines in Nrf2

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14
Q

where is NQO1 found

A

tree bark

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15
Q

what does Nrf2 act as a suppressor of

A

pro-inflammatory responses and skin carcinogenesis

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16
Q

what causes skin inflammation

A

exposure to SSUV radiation

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17
Q

what protects against SSUV radiation-mediated inflammation

A

genetic activation of Nrf2

18
Q

what does chronic exposure to SSUV radiation cause in mice

A

formation of tumours in SKH-1 hairless mice (which closely resemble histologically human cutaneous squamous cell carcinoma)

19
Q

what is the median rate of point mutations in SNPs (single nucleotide polymorphisms)

A

7699 per case

20
Q

what percentage if C.G - T.A base pair transitions follow a pyrimidine base to dipyrimidine oncogenic photoproducts

A

81.6%

21
Q

how is Nrf2 pharmacologically activated

A

by TBE-31

22
Q

what is azathioprine and what does it do

A

an immunosuppressive drug which aids in organ transplants

23
Q

what protects against SSUV radiation-mediated skin carcinogenesis

A

genetic activation of Nrf2 by lowering the expression of Keap1 (Keap1-KD)

24
Q

what happens in Nrf2-deficient mice

A

the protective effects of loweing the expression of Keap1 is lost

25
Q

what linerally correlates with the inhibition of pro-inflammatory responses

A

pharmacological Nrf2 activation

26
Q

what protects against SSUV radiation-mediated inflammation and skin carcinogenesis in mice

A

pharmacological or genetic nrf2 activation

27
Q

what is itaconate

A

an anti-inflammatory metabolite and an endogenous Nrf2 activator

28
Q

what causes the accumulation of itaconate

A

LPS stimulation of macrophages

29
Q

what is itaconate a product of

A

the TCA cycle

30
Q

what is itaconate involved in

A

it is weakly electrophilic and is involved in LPS-mediated stabilization of Nrf2

31
Q

what is a sensor for 4-octyl itaconate

A

C151 in Keap1

32
Q

how does itanocate activate Nrf2

A

via alkylation of Keap1

33
Q

what does Nrf2 activation potentiate

A

macrophage responses to LPS, favouring pathogen inactivation/clearance whilst attenuating IL1B pro-inflammatory signalling

34
Q

what is 4-octyl itaconate and what does it atcivate

A

a cell permeable analog of endogenous metabolite itaconate which activates Nrf2

35
Q

how does 4-octyl itaconate activate Nrf2

A

it causes 2,3-dicarbocypropylation of Keap1

36
Q

where are Nrf2-target genes suppressed

A

in COVID-19 patient biopsies

37
Q

what counteracts SARS-CoV2 infection

A

4-octyl itaconate

38
Q

wich type of cells have a low transition probability into later stages of HSV1 infection

A

cells with a high level if transcripts of Nrf2-target genes, and therefore high Nrf2 activity

39
Q

what do cells at later stages of infection respond by doing

A

increasing transcription of Nrf2-target genes

40
Q

what does increasing transcription of Nrf2-target genes do

A

could reflect a cellular defense mechanism against HSV1 infection

41
Q

what counteracts HSV1 infection

A

pharmacological activation of Nrf2 with bardoxolone methyl or sulforaphane

42
Q

what happens when viruses (such as HSV1 and SARS-CoV2) inactive Nrf2

A

they use this as a mechanism to enhance their own propagation

cell proliferation (12 decks)

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