lecture 19 redone Flashcards

1
Q

heterogeneity

A

each component can have multiple isoforms e.g different isoforms of IP3 and RyR receptors

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2
Q

2 types of remodelling

A

phenotypic remodelling
genotypic remodelling

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3
Q

phenotypic remodelling

A

when a component becomes phosphorylates
alters transcription rate so more/less of it is produced

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4
Q

genotypic remodelling

A

mutation in the gene that is encoding to isoforms and alters the activity

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5
Q

phenotypic remodlling in the heart:
adrenaline binds to its receptor in the heart cells it elevates

A

cAMP

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6
Q

cAMP causes phosphorylation of

A

calcium signalling components (voltage operated calcium channel and SERCA), causes larger calcium transient - stronger heart contraction

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7
Q

phenotypic remodelling in the liver:
if liver gets damages it will down regulate

A

key calcium signalling components

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8
Q

lower frequency calcium spikes of greater duration

A

has lower numbers of vasopressin receptors and IP3Rs whilst the liver regenerates

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9
Q

phenotypic and genotypic remodelling can be negative though and causes disease e.g.

A

alzheimers disease (phenotypic) brodys disease (genotypic)

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10
Q

alzheimers disease
beta-amyloid oligomers increase calcium entry via the

A

NMDA receptor

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11
Q

also the amyloid precursor protein (APP) intracellular domain (AICD) which

A

increases calcium release from stores

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12
Q

amyloid precursor protein is in the membrane and in AD the Abeta monomers come together into oligomer and the oligomer binds to the

A

NMDA receptor

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13
Q

the oligomer binding to the NMDA receptors allows

A

more calcium to enter the cell

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14
Q

the AICD on the precursor protein gets chopped off into the cytosol and enters nucleus where it is a

A

transcription factor

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15
Q

the AICD increases the transcription of the

A

RyRs

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16
Q

the AICD decreases the transcription of

A

calbindin (buffer)

17
Q

memories are triggered by

A

calcium entry (1000nM) through the NMDA receptor

18
Q

calcium entry (1000nM) through the NMDA receptor is known as

A

LTP (long term potentiation)

19
Q

when memories enter initially they enter the

A

temporary memory store

20
Q

over night all these memories get

A

consolidated into permanent memory store

21
Q

then we get a broader calcium signal (300nM) which triggers

A

LTD (long term depression)

22
Q

LTD erases what

A

erases the temporary memory store so it can receive new temporary memories

23
Q

memory in AD
resting calcium level is increase from 100nM to 300-500nM
we still get LTP laying down the temporary memory but because the resting level is increased we have

A

persistent activation of LTD

24
Q

persistent activation of LTD causes

A

erasure of the temporary memory store before the memories can be consolidated into permanent memory store

25
Q

we could try increase the expression/efficacy of the

A

off mechanisms

26
Q

what vitamin does this

A

vitamin D

27
Q

vitamin D

A

increase expression of calcium ATPases
sodium calcium exchanger
increases concentration of calbindin

28
Q

there is a bidirectional relationship between

A

calcium signalling and the amyloidogenic pathway

29
Q

calcium signalling simtulates

A

the metabolism APP