2.6 Flashcards

(33 cards)

1
Q

inhibition of cellular gene expression by several viral proteins (5)

A

inhibition of transcription by RNA polymerase 2
inhibitbition of polyadenylation
inhibition of RNA export
Inhibition of translation
increase mRNA degredation

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2
Q

what increased rates increase mRNA (3)

A

transcription by RNA pol 2
polyadenylation and splicing
nuclear export

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3
Q

what increased rates decrease mRNA (3)

A

intrinsic turnover
microRNA - promoted degredation
nonsense mediated decay

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4
Q

what gets the eIF4E complex and everything (the ribosome) moving (to look for AUG) and scanning for translation

A

the hydrolysis of ATP to ADP

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5
Q

what cat happens without eIF4E

A

host translation

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6
Q

what do PKR and PERK have

A

kinase activity

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7
Q

what do PKR and PERK do

A

phosphorylate eIF4a

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8
Q

the integrated stress response

A

cellular sigbnals that lead to global shut off of cellular translation initiation through the phosphorylation of eIF2a

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9
Q

what happens when eIF2a is phosphorylated

A

it gets stuck (tightly binds) in eIF4B and translation initiation is inhibited

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10
Q

what is eIF2a

A

forms the complex between tRNA-met and GTP to deliver the initiator tRNA to the 40s ribosome unit

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11
Q

how does eIF4B initiate translation

A

it recycles eIF2a’s GDP to a GTP so eIF2a can recruit the tRNA-Met complex

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12
Q

what pathway can viruses activate to inhibit apoptosis and promote translation

A

ATK

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13
Q

activation of PI3K pathways do what

A

induce clathrin coasted pits and endocytosis

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14
Q

3 menthods of virus activation of entry pathways listed

A

activation of PI3K to induce clathrin coasted pits
allow for membrane fusion by upregulation of RAC
induce cluttering and signalling by lipid rafts to also enhance entry

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15
Q

what does RAC do

A

makes the membrane more flexible and ready for fusion

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16
Q

3 inhibition of cellular gene expression by several viral proteins

A

inhibition of transcription of RNA pol 2
inhibition of translation
increase mRNA degradation

17
Q

3 things needed to initiate translation

A

the eIF2-tRNA-Met complex
eIF4E
the hydrolysis of ATP to ADP

18
Q

do hosts shut off translation to try and counteract a virus

A

yes, so this virus needs a way to try and inhibit this

19
Q

what does PERK respond to

A

overload of proteins in the ER

20
Q

what does PKR respond to

A

viral infection - dsRNA

21
Q

how many PKR’s are needed to bind dsRNA and induce phosphorylation

22
Q

does PKR need to be autophosphorylated first

A

yes its autophosphorylated when it binds the dsRNA and then its ready to phosphorylate eIF2a

23
Q

3 eIF2a kinases

24
Q

what is GCN2 induced by

A

amino acid starvation

25
what does delta E4 do
it pushes the cells metabolism to the consumption of glucose
26
why do viruses benefit from glucose
they have to make lots of things in the cell and most of them require ATP and energy to do. it needs enough ATP to fuel these processes
27
do all viruses push the same metabolism
no they push what they depend on for its needs (either fatty acids, glucose, or acetyl CoA)
28
major hub of carbon metabolism
TCA cycle
29
what cycle leads to precursors to synthesis of many biomolecules
TCA cycle
30
source of energy is stored in most organisms in
lipid droplets
31
any virus that wants to make more fat will turn on what pathway
SREBP1
32
what is SREBP1
transcription activator that turns on genes for fatty acid synthesis
33
how does SREBP1 enter the nucleus
HCMV activates mTOR1. Activated mTOR1 phosphorylates Lipin 1 and then the phosphorylated Lipin 1 cannot inhibit SREBP1 - therefore leading to SREBP1 entering the nucleus and the expression of genes for fatty acid synthesis