Author: mfadmin

Cytochrome P-450,”enzymes that modify smoked meat compounds(why liver cancer is so prevalent)liver exposed to higher concentration of these compounds than other organs and tissuesIntestinal epithelial cells (exposed to everything that goes through our bodies)cytochrome P-450 convert, guanine forms covalent adduct that can only be repaired by DNA repair enzymes

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Cytochrome P-450,”enzymes that modify smoked[…]

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With exposed regions of DNA…,”only have exposed DNA very transiently during transcription and replicationModified guanine will distort double helix, will be enough to activate themRNA polymerase can’t get through them, going to have exposed regions of DNA single stranded DNA activates kinasesKinases have two main targets to phosphorylate:1) P532) checkpoint 1 or 2Going to see:1) stop cell cycle2) activate expression of gene3) if none work

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.With exposed regions of DNA…,”only[…]

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ATM Kinase,”stress-activated kinasestarting point: have very little p53 in our cells (it is a constitutively active gene) b/c cells have specific ubiquitin ligase that targets p53 (Mdm2)directly phosphorylates p53, this phosphorylation stabilizes it. P53 acts as a tetramer (levels starting to rise…have to allow concentration to rise where it can work)have to get Mdm2 out of the way, so ATM also phosphorylates Mdm2, which activates ___ ligase activity (arf?)stabilizing p53 phosphorylation, inactivating ubiquitin ligase to get it out of the way (so p53 levels can increase–>p53 DNA binding protein has different sequences that it binds to w/ different affinities)P53 sites associated with P21cip (stops cell cycle wherever DNA damage takes place, but doesn’t stop damage)activates genes encoding proteins that can fix the damage (once p53 gets to intermediate levels) and if damage fixed, inactivate ATM, shut off kinase, phosphatases come in, dephosphorylate p53, and dephosphorylate Mdm2shuts off P21cip, cell cycle takes off, back to normalif damage ISN’T fixed, p53 levels keep rising

Biology

Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.ATM Kinase,”stress-activated kinasestarting point: have[…]

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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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