replicative immortality Flashcards
how many copies of each gene in a cell
2
what are post-translational modifications
covalent modification of proteins following synthesism they are critical in cell signalling
3 common post-translational modifications
phosphorylation, glycosylation, carbonylation
which amino acids can be phosphorylated through phosphodiester bonds
serine, threonine, tyrosine
which amino acids can be phosphorylated through phosphoramidite bonds
histidine, lysine and arginine
what do phosphotransferases (e.g. kinases) do
add phosphate
what do phosphatases do
remove phosphate
what does cell mortality mean
cells only have the ability to divide a certain number of times, they stop growing after a certain number of doublings
cell senescence
cells stop growing after a certain number of doublings, cells are in G0 and have left cell cycle. cells are metabolically active and are viable
how can cell senescence be circumvented (avoided)
by disabiling TSG’s pRb and p53, cells can keep doubling until they reach ‘crisis’
what does it mean for a cell to reach ‘crisis’
massive cell death, karyotypic disarray associated with end-to-end fusion of chromosomes
what does p53 do when cells have serious DNA damage
it promotes apoptosis to limit the transfer of damaged DNA
what does the Rb (retinoblastoma) gene do
stops excessive cells growth by inhibiting the cell cycle progression until the cell is ready to divide
how and when is Rb inactivated
it is phosphorylated when the cell is ready to divide
what is the Hayflick limit
the replicative limit of normal cells is related to the number of doublings (DNA replication)
what happens to cells when they are unfrozen (in terms of doubling)
they remember the amount of doublings they have left
what are telomeres
hexameric repeats that shorten after each DNA doubling
why do telomeres get shorter over time
they cannot be complete replications of the DNA, each time some bases cant be replicated
what happens when the telomeric DNA gets too short
it is unable to protect the chromosomal DNA and the unprotected chromosomal ends participate in end-to-end chromosomal fusions which characterise ‘crisis’
what is telomerase
ribonucleoprotein enzyme terminal transferase
what happens in cancer to avoid telomere shortening
telomerase extends the 3’ end on telomeres to elongate them with hexanucleotide repeats
what does over expression of hTERT prevent
shortening of the telomeres and therefore replicative crisis
