progeria
premature aging- prob with nuclear lamina
in regard to lamina, what happens during interphase
it disassembles and is phosphorylated
what happens with the lamina during telophase?
reassembles
Papillary thyroid cancer gives nuclei with:
clear nuclei- orphan annie eye nuclei
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
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
what happens in mitosis
division of the nucleus
what happens in the s phase
duplication of chromosomes
in what phases are centrioles replicated
start and finish
starts at g1- ends at g2
what do germinal cells possess that allow the to not reach senescence?
what also has this?
telomerase
cancer cells
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
what flags a cell for apoptosis
phosphotidyl serine is moved from cytoplamic side to extracellular side to signal apoptosis
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
Fas
a death receptor
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
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