Lecture 8 Flashcards Preview

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Flashcards in Lecture 8 Deck (16):
1

progeria

premature aging- prob with nuclear lamina

2

in regard to lamina, what happens during interphase

it disassembles and is phosphorylated

3

what happens with the lamina during telophase?

reassembles

4

Papillary thyroid cancer gives nuclei with:

clear nuclei- orphan annie eye nuclei

5

what are the three components of the nucleolus

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

6

nucleostemin

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

7

what happens in mitosis

division of the nucleus

8

what happens in the s phase

duplication of chromosomes

9

in what phases are centrioles replicated
(start and finish)

starts at g1- ends at g2

10

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

telomerase
cancer cells

11

necrosis vs apoptosis

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

12

what flags a cell for apoptosis

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

13

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

intrinsic- when there is cell damage, uses mitochondria
extrinsic- uses caspases and cytochrome C and receptors like FAS which is a death receptor

14

Fas

a death receptor

15

Fas ligand counter attack

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

16

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

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