How dominant-negative mutations caused p53 to also be identified as an oncogene,”most p53 mutations eliminate DNA binding and destabilize the protein (mutant protein is functionally “”invisible””)BUT since p53 functions as a tetramer, some mutations that eliminate p53 function (transactivation), also inactivate tetramers containing only 1 mutant subunitIf cells contain equivalent amounts of wild-type and d-n mutant forms of p53 protein

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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

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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