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Checkpoints 1 and 2
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Checkpoints 1 and 2 inhibit[…]
Read more“Normal vs “”transformed”” cells”
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.“Normal vs “”transformed”” cells” normal[…]
Read moreHW: Burkitt’s lymphoma is due to the overexpression of c-myc protein. Chronic myelogenous leukemia (CML) is due to the expression of constitutively active Bcr-Abl protein. What do these two cancers have in common?
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.HW: Burkitt’s lymphoma is due[…]
Read moreATM 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
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.ATM Kinase,”stress-activated kinasestarting point: have[…]
Read moreProfactory requirements
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Read moreHW: What was the basis for finding that Axitinib could be used to treat Gleevec-resistant CML?,”Axitinib is a previously well-characterized and effective VegFR inhibitor that binds with a high affinity to Bcr-Abl (T315I)
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Read moreMdm2,”p53-specific ubiquitin ligasephosphorylated by ATM, causing it to bind to Arf, takes it to nucleolis (site of ribosome production
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.Mdm2,”p53-specific ubiquitin ligasephosphorylated by ATM,[…]
Read moreAnchorage Dependence
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Read moreP53,”most important tumor suppressorthe weak point of the system-the single point of failure; p53 is protein that links DNA damage to activating the checkpoint throughout the cycle (because DNA damage can occur at any time), stopping the cell cycle, repairing the damage and initiating apoptosis(interactions with ATM kinase, Mdm2, and Chkpoints1&2)In low concentration, p53 stops cell cycle. Damage unstopped b/c don’t activate repair genes (not high enough affinity) damage persists, repair genes activated, cell cycle arrest transientIf inactivated, damage accumulates
Average Rating 0 out of 5 stars. 0 votes.You must log in to submit a review.P53,”most important tumor suppressorthe weak[…]
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