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

A
17
Q

Extrinsic Death Receptor-mediated cell death

A
18
Q

SELF STUDY

A
19
Q
A
20
Q
A
21
Q
A
22
Q
A
23
Q

Extrinsic Death Pathway & Disease

A
24
Q

explain the Control of cell death – Bcl-2 family

A

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
Q

describe the Bcl-2 family and their roles

A
26
Q

Apoptosis disrupts mitochondria (BH123 members)

A
27
Q

Bcl-2 prevents mitochondrial disruption

A
28
Q

BH3 only proteins inhibit Bcl-2 & tip the balance

A
29
Q

explain how CELL STRESS can affect the control of apoptosis

A

DNA (genotoxic) damage stabilizes p53 > production of BH3 only members (Bad, Bid, Noxa, Puma)
= PRO-DEATH

30
Q

explain how IAPs can affect the control of apoptosis

A

Inhibitors of Apoptosis (inhibit caspases = anti- death)
produced by some viruses to prevent death
Over-expressed in some cancers

31
Q

explain how Too little apoptosis INCREASED risk cancer

A

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
Q

what are the different levels of Cell death machinery can be inactive

A

Over-expression of anti-apoptosis genes
Modulation of caspases
Mutation of pro-apoptotic genes
Alteration of cell death regulators

33
Q

what can occur when there is an Over-expression of anti-apoptosis genes bcl-2 and follicular lymphoma

A

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
Q

what can occur when there is an Over-expression of anti-apoptosis genes c-myc gene (cell cycle)

A

Chromosome 8
Translocated to chromosome 14 close to Ig heavy chain enhancer → high expression
Proliferation of cells

35
Q

what can occur when there is an Over-expression of anti-apoptosis genes c-myc and bcl2

A

speed the formation of lymphoma

36
Q

are all pro-survival Bcl-2 family members predicted to be oncogenes

A

yes

37
Q
A