Category: Biology

BIO205

Telomerase inactivation,”cells become immortalized, but are not cancer cells (mouse cells) –>used to identify human oncogenes*took DNA of human tumors, added them to mouse cell lines that have already been immortalized. They aren’t tumor cells, but still require growth factorsBehavior of cells: telomeres are structures on end of chromosomes that have to be maintained every time cells replicatetelomerase expressed at high level (gets shut off very early (exception is stem cells))normal cells: telomere gets bit shorter each replication (50)In cancer cells: telomerase gets reactivated, but not properly regulated. telomeres get too large. Don’t become senescent; but undergo chromosomal rearrangement (lose p53)*took normal cells, try to very carefully reactivate telomerase to become cancer cells

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Telomerase inactivation,”cells become immortalized, but[…]

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Ames Test,”demonstrates that carcinogens (cause cancer) are mutagens (alter DNA)Ames introduced a mutation into a single gene that required Histodine Biosynthesis. This strain of bacteria called His-Auxotroph.Have to add histodine b/c cells can’t make it on its own. Wanted to see what it takes to get cells from His-auxotroph to His-prototroph. These cells have very specific type of genetic mutation, so added compound must be specific mutagen that will mutate DNA at high enough frequency that mutation you’ll get will be able to restore to the original mutationif strong mutagen, lots of coloniesif weak or poor mutagen, will not see anything(a lot of compounds, if first incubated with liver extract

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Ames Test,”demonstrates that carcinogens (cause[…]

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Caspase Cascade,”involving interplay between metabolism, especially w/ mitochondria, and the nucleushappens only in presence of P53-p53 first shuts off survival of BCL2, activating expression of Apaf 1 (apoptosome), increases expression of Caspase-9, then increases expression of Caspase 3,-7All inactive, so all p53 is doing is increasing their levels (not activating them yet)p53 increase levels of ribonucleotide reductase (RR) & BAX1 which increase cytosolic levels of dATP and Cyt c, respectivelymoving into apoptosis: RR remaining active, continue rerouting deoxynucleotides to ribonucleotides? Ribodeoxy ATP*all cytochrome c going to leak out in cytoplasm, so mitochondria all deadcytochrome C works with deoxy ATP and now big pool of Apaf1 that p53 madenow activating Apaf1, cytochrome C and deoxy ATP activated (no kinases here…all enzymatic signaling)As we start turning Caspases 3 and 7 on

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Caspase Cascade,”involving interplay between metabolism,[…]

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