apoptosis, programmed cell death Flashcards

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1
Q

how do you control your organs sizes?

A

cell growth, cell division, cell death

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2
Q

examples of apoptosis during development?

A

sculpting, deleting structures, adjusting cell numbers

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3
Q

what disease if there is too much apoptosis?

A

alzheimers

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4
Q

disease if too little apoptosis?

A

cancer and autoimmune disorders

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5
Q

example ff apoptosis bing hijacked?

A

virus, bacteria

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6
Q

to get cancer, what two things have to be present

A

deregulated cell proliferation ALONG WITH suppressed apoptosis

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7
Q

what is necrosis

A

degeneration of all cellular organelles, and spewing contents by rupturing the plasma membrane into the environment

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8
Q

apoptosis vs necrosis

A

apoptosis condenses the chromatin and is controlled. the mitochondria in apoptosis are also not swelling and popping, unlike necrosis

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9
Q

early look of an apoptosing cell

A

it “rounds up” because the cytoskeleton is broken down by proteolysis
ie. it used to be a flat and happy fibroblast, and now it looks round and has condensed chromatin

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10
Q

what is blebbing? what does it do?

A

blebbing is breaking apart of the cell in a CONTROLLED manner. it allows a phagocyte or neutrocyte to recognize death and eat the cells

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11
Q

what regulates effectors? example of effector

A

sensors signal things like protease “capsase”

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12
Q

__are the things that keep a cell in its happy place

A

trophic growth factors (PDGJ,NGF,IGF,IL). if these are MISSING then apoptosis is initiated

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13
Q

what signals a cell to murder another cell?

A

presence of fas ligand or TNF stimulates apoptosis

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14
Q

so there are two ways to signal death. do the different signals have different results.

A

nope. death, by same mechanism

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15
Q

famous cancer related gene?

A

p53. it is a tumor supressor. if you don’t have it, you can’t trap the cell in G0 phase

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16
Q

4 things that cause cell death

A

DNA damage, signal imbalance, lack of survival factor, hypoxia

17
Q

what are capsases

A

downstream effectors of cell death that destroy lamins, cytoskeletons

18
Q

how are capsases stored

A

stored in an inactive state and are activated by something before they work

19
Q

most upstream capsase? activated by?

A

procaspase 9 which needs proteolysis by two things that associate

  • Cytochrome C (normally in mito)
  • Apaf-I
20
Q

what is the general organization of capsase action

A

caspase cascade

21
Q

wheel of death is? made of ? does?

A

apoptosome. its made of lots of cytC it brings in capsase 9

22
Q

what is the signal for capsase 9

A

cyt C

23
Q

what signals the cyt C to come out of the cell?

A

BCL-2 family of protein. but this family is “YING/YANG” some of them are antipoptotic, some are proapoptotic

24
Q

what are the proapoptotic BCLS?

A

baX or baK. they letthe cytC out (of the mitochondria)

25
Q

what are the antiapoptotic BCLS?

A

BCL-2 or BCL-XL; it binds bak or bax to keep it from coming together and making a pore that lets Cyt C out

26
Q

what does Bad do?

A

he is bad and he prevents the BCL-2 and BCL-XL to come together to prevent cell death…. (inhibits the inhibitor) so it apoptoses

27
Q

what prevents Bad from doing its job

A

phosphorylation

28
Q

what does bim do.

A

it prevents bcl-2 binding and is released by disruption of microtubule cytoskeleton. it stimulates cell death

29
Q

how does a growth factor affect Bad?

A

the cell makes a 14-3-3 protein and phosphorylates Bad

30
Q

where does puma come from?

A

it comes out of the nucleus when there is DNA damage to stimulate bak and bax

31
Q

what upregulates BCL-XL? how does this work in hemopoeisis?

A

epo. keeps the cells from dying even though the nucleus is destroyed

32
Q

if you upregulate BCL-2?

A

keeps the cell alive…. even if it shouldn’t be