Cell Death Flashcards

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1
Q

How does cell cycle arrest occur?

A

DNA Damage results in p53 phosphorylation
• p53 stimulates transcription of p21(Cdk inhibitor protein)
• Results in cell cycle arrest.
• Under normal conditions p53 is degraded so the cell cycle can proceed.

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2
Q

What is caused by overexpression of Myc?

A

Our cells prevent cancer by inhibiting Mdm2, leading to the production of active p53. • p53 causes cell cycle arrest or cell death (apoptosis).

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3
Q

What is the difference between mitosis and meiosis?

A

Mitosis happens in somatic cells, same number of chromosomes as starting cell (diploid) Needed for growth and repair.
Meiosis occurs in germ cells, Half # chromosomes as starting cell (haploid) • Needed for sexual reproduction

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4
Q

Describe how homologous pairs line up and separate in meiosis

A

They line up on the spindle and separate and anaphase 1, sister chromatids separate at anaphase 2.

Mitosis - duplicated chromosomes line up individually

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5
Q

How to kinetochores on sister chromatids attach in mitosis and meiosis?

A

Mitosis - they’re attached to diffrent poles. Meiosis - attached to same pole.

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6
Q

What are the types of cell death?

A

Programmed - cells kill themselves in a controlled way, necrosis - cells swell and burst in response to insult.

Cell death can occur to help development.

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7
Q

Describe apoptosis -

A

One type of programmed cell death.
Depends on cascade of degradation enzymes called caspases.
Cytoskeleton disassembly, breakdown of nuclear envelope, and DNA is cleaved. •

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8
Q

Describe caspase activation during apoptosis -

A

caspases are activated by cleavage to cause apoptosis. Activation of initiator caspase by apoptotic signal causes executioner caspase to be activated by cleavage, leading to apoptosis.

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9
Q

Describe the extrinsic pathway of apoptosis -

A

activated by a signal from outside target cell, fas ligand binds to fas death receptor, causing DISC to assemble. Cleavage and activation of caspase 8 occurs, activating executioner caspases and leading to apoptosis.

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10
Q

Describe the intrinsic pathway of apoptosis -

A

activated by a signal from inside the target cell, release of cytochrome c in intermembrane space, activating Apaf1,
CARD domains come together assembling apoptosome, caspase 9 recruited and activated, executioner caspases activated, leading to apoptosis.

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11
Q

Describe anti-apoptotic bcl2 proteins -

A

maintains membrane integrity, keeps cytochrome c in cell, bax/back is inactive.

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12
Q

What happens when BH3 only protein is activated by apoptotic stimulus?

A

anti apoptotic Bcl2 protein turneed off, BaxBak protein activated, come together to let cytochrome c move out.

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13
Q

Describe inhibitors of apoptosis -

A

Bind and inhibit activated caspases • Anti-IAPs prevent IAPs from binding caspases.

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14
Q

How do Anti-IAPs work?

A

They are released to prevent IAPs from interfering with apoptosis.

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15
Q

What survival factors inhibit apoptosis?

A

increased production of anti-apoptotic Bcl2 protein, inactivation of pro apoptotic BH3 only protein, inactivation of anti IAPs

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