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PSC2002 Membrane Transport & Cell Signalling > PSC2002/L20 Calcium Signalling IV > Flashcards

PSC2002/L20 Calcium Signalling IV Flashcards

1
Q

Give the 3 types of RyR receptor and where they are found.

A

Type I - skeletal muscle
Type II - cardiac muscle
Type III - brain

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2
Q

What is the difference between the 3 IP3 isoforms?

A

Different affinities for IP3 and calcium
CICR occurs at different times

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3
Q

What are the differences between receptor isoforms on different cells?

A

Affinity
Stability
Cellular localisation

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4
Q

What is the signalsome?

A

Toolkit for calcium signalling in a specific cell
Includes specific isoforms involved in on/off mechanism

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5
Q

Give the 6 components of the calcium signalling toolkit.

A

Receptors
Transducers
Channels
Pumps
Buffers
Sensors

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6
Q

Describe a cardiac specific calcium signalsome.

A

ON - Et-1R, PLCbeta1, L-type; RYR2
OFF - SERCA2a, PV
Sensors - CAM, TnC

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7
Q

Describe a T cell-specific calcium signalsome.

A

ON - TCR; IL-2R, PLCy1; PI 3-K
OFF - SERCA2b, CR
Sensors - CAM

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8
Q

Define and give an example of phenotypic remodelling of the signalsome.

A

Txn rate increased or decreased
E.g., phosphorylation can change activity of a component; altered txn rate of component

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9
Q

Define and give an example of genotypic remodelling of the signalsome.

A

Change due to inherent event with protein
E.g., somatic mutations in single cells alters activity of component
Germline mutations passed from one generation to next

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10
Q

When does phenotypic remodelling occur?

A

Under normal conditions for normal operation of the cell

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11
Q

Describe phenotypic remodelling in the heart during exercise.

A

Increased force of contraction with exercise
cAMP-dependent reversible phosphorylation of key Ca2+ signalling components (e.g., VOC, SERCA) enables heart cells to generate larger Ca2+ signals
Increased L-type and SERCA2a

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12
Q

Describe phenotypic calcium remodelling in the liver during regeneration.

A

Down-regulation of key Ca2+ signalling components results in lower frequency Ca2+ spikes of greater duration

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13
Q

What kind of calcium remodelling is involved in:
a) Alzheimer’s Disease
b) Brody’s Disease?

A

a) phenotypic signalsome
b) genotypic signalsome

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14
Q

Describe the pathogenesis of Alzheimer’s Disease. (4)

A

Extracellular plaque deposits of B-amyloid disrupts synaptic transmission
AB increase Ca2+ entry via NMDA receptor
Amyloid precursor protein (APP) intracellular domain (AICD) increased Ca2+ release from stores
Upregulation of neuronal Ca2+ signalling to induce initial decline in memory

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15
Q

Give 3 binding sites on NMDA receptors.

A

Glycine site
Channel pore
Zinc site
Proton site
Glutamate site
Polyamine site

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16
Q

What is a NMDA receptor?

A

Non-specific cation channel
Large Ca2+ component

17
Q

Describe the change in Ca2+ during Alzheimer’s pthogenesis. (2)

A

Overexpression of RyR so increase Ca2+ leak
Decrease in Ca2+ buffering through calbindin

18
Q

What is the normal level of resting Ca2+ and what does this increase to during AD?

A

100nM to 300-500nM

19
Q

Describe normal memory storage. How is this different in AD?

A

Ca2+ entry through NMDA receptor
Memory formation (LTP) to temporary memory store
Memory consolidation into permanent memory store
Long term depression erases temporary memory store

20
Q

Describe memory formation in AD. (2)

A

Long term depression occurs throughout so temporary memories erased before they become permanent
Amyloid metabolism enhances resting level of calcium

21
Q

Give an alternative name for:
a) LTP
b) LTD.

A

a) memory storage
b) memory loss

22
Q

Give a potential therapy for reversing Ca2+-dependent neurodegeneration.

A

Vitamin D3 acts as TF for many OFF mechanisms
Bringing down calcium baseline

23
Q

Describe how onset and progression of AD can be described as positive feedback.

A

Ca2+ signalling stimulates metabolism of APP
Amyloidogenic pathway increases resting Ca2+

24
Q

What is Brody’s Disease (myopathy)?

A

Skeletal muscle genetic disorder characterised by stiffness and cramp brought on by prolonged Ca2+ elevation and slowing of relaxation

25
Q

How is Brody’s disease caused?

A

Defect results from mutation in SERCA1 pump
SR unable to refill with Ca2+
Cytosolic Ca2+ remains elevated so relaxation impeded

26
Q

Give 2 examples of Ca2+ signal remodelling in cancerous cells.

A

Altered SERCA pump activity
Altered Ca2+ release through InsP3Rs
Altered resting level of Ca2+

27
Q

What is the cause of cancer with relation to Ca2+?

A

Unknown whether Ca2+ signal remodelling is a consequence of cancer or helps to cause cancer
Due to bidirectional relationship between them

28
Q

Describe the bidirectional relationship between Ca2+ signalling and cancer.

A

Ca2+ signalling remodelling causes changes in cellular activity
Cancer (changes to cellular activity) causes remodelling of Ca2+ signals

PSC2002 Membrane Transport & Cell Signalling (25 decks)

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