Apoptosis Flashcards

1
Q

true or false apoptosis is highly conserved

A

true

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2
Q

what is apoptosis crucial for

A

development
maintenance
control

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3
Q

what can occur when apoptosis is overreactive

A

Neurodegeneration
Immunodeficiency
Stroke
Transplant Rejection

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3
Q

what can occur when apoptosis is under reactive

A

Neurodegeneration
Immunodeficiency
Stroke
Transplant Rejection

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4
Q

what can occur when apoptosis is overreactive affecting the life-death balance

A

Allows cell accumulation (e.g. accumulation of cells during an immune response)

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5
Q

what can occur when apoptosis is under reactive affecting the life-death balance

A

Returns cell populations to normal after challenge
Neutrophil apoptosis during inflammation

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6
Q

phases of apoptosis

A
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7
Q
A
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8
Q
A
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9
Q
A
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10
Q
A
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11
Q
A
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12
Q

describe the Cleavage of caspase substrates in Apoptosis

A
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13
Q

what is the extrinsic pathway

A

Cell are instructed to die from outside
Receptors (“Death Receptors”) on cell surface induce death when ligated

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14
Q

what is the intrinsic pathway

A

Intracellular Insults can induce

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15
Q

why are apoptosis molecules important

A

important in recruiting initiator caspases and allowing their activation

16
Q

Intrinsic Pathway-mediated cell death

17
Q

Extrinsic Death Receptor-mediated cell death

18
Q

SELF STUDY

23
Q

Extrinsic Death Pathway & Disease

24
explain the Control of cell death – Bcl-2 family
Family of interactive proteins Protect from apoptosis – Pro-survival Suppress protection – Pro-death Pro- death and pro-survival members Bcl-2 - prototypic member of the family
25
describe the Bcl-2 family and their roles
26
Apoptosis disrupts mitochondria (BH123 members)
27
Bcl-2 prevents mitochondrial disruption
28
BH3 only proteins inhibit Bcl-2 & tip the balance
29
explain how CELL STRESS can affect the control of apoptosis
DNA (genotoxic) damage stabilizes p53 > production of BH3 only members (Bad, Bid, Noxa, Puma) = PRO-DEATH
30
explain how IAPs can affect the control of apoptosis
Inhibitors of Apoptosis (inhibit caspases = anti- death) produced by some viruses to prevent death Over-expressed in some cancers
31
explain how Too little apoptosis INCREASED risk cancer
cells don’t die and accumulate cancer fails to respond to treatment malignant cells fail to die in response to ->chemotherapy ->immune surveillance (e.g. by T cells and NK cells)
32
what are the different levels of Cell death machinery can be inactive
Over-expression of anti-apoptosis genes Modulation of caspases Mutation of pro-apoptotic genes Alteration of cell death regulators
33
what can occur when there is an Over-expression of anti-apoptosis genes bcl-2 and follicular lymphoma
Chromosome 18 Translocated to chromosome 14 close to Ig heavy chain enhancer →high expression Suppression of apoptosis → lymphoma T(14:18) characteristic of follicular lymphoma
34
what can occur when there is an Over-expression of anti-apoptosis genes c-myc gene (cell cycle)
Chromosome 8 Translocated to chromosome 14 close to Ig heavy chain enhancer → high expression Proliferation of cells
35
what can occur when there is an Over-expression of anti-apoptosis genes c-myc and bcl2
speed the formation of lymphoma
36
are all pro-survival Bcl-2 family members predicted to be oncogenes
yes
37