Lecture 8 Flashcards

(16 cards)

1
Q

progeria

A

premature aging- prob with nuclear lamina

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2
Q

in regard to lamina, what happens during interphase

A

it disassembles and is phosphorylated

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3
Q

what happens with the lamina during telophase?

A

reassembles

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4
Q

Papillary thyroid cancer gives nuclei with:

A

clear nuclei- orphan annie eye nuclei

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5
Q

what are the three components of the nucleolus

A

1) nucleolar organizer DNA
2) Pars fibrosa- newly transcribed rRNA starting to be complexed with protein
3) pars granulosa- maturing subunits of ribosomes

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6
Q

nucleostemin

A

binds p53 in undifferenciated cells (remember: stem is the beginning and thus undifferentiated)
may play a role in unchecked proliferation cancer cells because nucleostemin binds p53, taking it up and preventing it from doing it’s proliferation checks

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7
Q

what happens in mitosis

A

division of the nucleus

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8
Q

what happens in the s phase

A

duplication of chromosomes

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9
Q

in what phases are centrioles replicated

start and finish

A

starts at g1- ends at g2

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10
Q

what do germinal cells possess that allow the to not reach senescence?
what also has this?

A

telomerase

cancer cells

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11
Q

necrosis vs apoptosis

A

apoptosis is regulated under immune surveillance and eliminates itself on purpose and don’t get an inflammatory response- eliminate via phagocytosis with macrophages or professional phagocytosis cells
vs
necrosis that happens violently with an inflammatory response

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12
Q

what flags a cell for apoptosis

A

phosphotidyl serine is moved from cytoplamic side to extracellular side to signal apoptosis

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13
Q

what are the types of apoptosis? which one is triggered when?

A

intrinsic- when there is cell damage, uses mitochondria

extrinsic- uses caspases and cytochrome C and receptors like FAS which is a death receptor

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14
Q

Fas

A

a death receptor

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15
Q

Fas ligand counter attack

A

done by cancer cells; express FAS and interact with immuno cells and bind with the FAS receptors there and kill them

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16
Q

why is the risk for osteoporosis so much higher post menopause?

A

in osteoblasts we have BAD (that is bad) which is a pro-apoptotic growth factor that promotes apoptosis of osteoblasts (no bone growth).
BUT we can change it to good (BAD-P) via estrogen via phosphorylation.
after menopause, we dont express as much estrogen so we can’t change BAD into BAD-P so you get osteoporosis