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22 Cards in this Set
- Front
- Back
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what balances each other and dictates total number of certain type of cell in a tissue? (3) |
mitosis?/proliferation
differentiation apoptosis
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what 2 things could disrupt this? what kinds of cancers does second this occur in? what results? |
overproliferation/lack of differentiation leukemias too many of one type of cell and not enough of another |
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who gave the first morphological description of apoptosis? what steps did he describe in apoptosis? |
Walter flemming Cell shrinkage from condensation (?) check word 15 min Budding of membranes Phagocytosis from the apoptotic bodies (guts of cells 15 min never get dumped into surrounding tissue so you don't get inflammation unlike some other thing??)(BAM?bomb?bom? as opp. of apoptosis cells swell, start leaking, break open and dump --> inflammation) |
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BCL2?maybe? is a _____ ______ regulates apoptosis by ______ release of ________ C from _______ KNOW INFO INSIDE ABOUT HOW MECHANISM OF BCL2 BLOCKS CYTOCHROME C |
survival factor inhibiting release of cytochrome c mitochondria |
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BAX AND BAC are pro-________ family members form the core thru which cytochrome c punches a ______ ______ in the ________ through which cytochrome C is released |
apoptotic regulated hole? |
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________2 binds to individual subunits, BAX and BAK`and keep them from forming the ____ |
BCL pore? core?-- anyway you need multiple subunits coming together to keep them from forming a pore/core and BCL2 keeps them from doing that |
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BIN and BIM (produced when cells are _______ and driven into apoptosis)bind to _______2 which keeps them from binding to ______ and ______ |
stressed BCL2 BAX and BAK |
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Frees up Bax and bak to make ______ (more, less) and to go into ________ |
more apoptosis (this one could be wrongly heard-- 18:18-- check) |
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Mic?? in addition to stimulating overepxpression can induce _________ ''these are counteirng each other, net effect being some increase in cell number'' but if something inhibits apoptosis gives you (big, small) ____ ant of cell increase |
apoptosis big |
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_______2 can inhibit apoptosis so effect of _____ + _____2 is more dramaticc than MIC overexpression alone |
BCL2 BCL2+MIC |
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what DNA tumor virus does oncogene come from ? what does it bind? (similar to how RB is bound by some of the oncoproteins from other tumors etf.) |
DNA tumor virus (SV40 virus??) |
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The onco protein large t-antigen from DNA tumor virus (SV40 Virus) (?)(20:12 ish) binds _______ in the same way that _______ is bound up by some of the DNA proteins from the other large tumor viruses its job?(whose?) |
p53 RB keep p53 from doing its job |
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p53 is lost/inactivated in ____% of all tumors tumors missing p53 survive more _______ so if you take a tumor that has an apoptotic response and treat with chemo or radiation it drives some cells into _______ but if it has lost p53 it has lost one of its major _______ pathways |
50 chemotherapy apoptosis apoptosis |
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p53 is a _______ ________ (in response to the function of p53) |
a transcription factor |
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p53 is induced by stress mild stresses induce ______ ________ _______ and ___ ______ _______ if something's wrong with growth cycle and you try to induce it-- if the stress is too bad it ---> _______ic protein |
growth arresting protein DNA repair protein apoptotic |
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since p53 can drive cells to suicide must be tightly regulated so that moderate stresses don't drive cells to go into apoptosis the really tight control of p53 is generated by _______2 = stressors increase p53, it's a TF inducing transcription of a number of different messages to produce a number of different proteins including (_____) which binds to p53 and accelerates its ___________ it is a ________ feedback to keep p53 from just taking off and killing itself inappropriately (so as stimulus is making p53 go up MDM2 is degrading some of that so that it doesn't go up so induced = when p53 rises MDM2 rises, binds to p53 and degrades part of its rise to keep it from running rampant) |
MDM2 degradation negative |
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things that induce p53 levels moderate responses induce p53 moderately and give you these responses severe |
hypoxia, mitotic apparatus disfunction, oncogene activation, telomere erosion, dna replication stress --> rise in p53 mod?- growth arrest, dna repair, antioxidant arrest scenesence or apoptosis 25 min ish |
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important because normal cell replicates giving you a perfect copy
dna damage if not _______ perfectly you don't want it to divide --> 2 damaged cells --> ___ levels go up, arrest in ____, make DNA ______ enzymes, problem fixed, cells go on and replicate normally and if they can't repair it they --> _____ -- this is the normal protective mechanism |
replicated p53 G1 repair apoptosis |
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in tumors there is no ______ so you don't get to _____ arrest cells divide carrying those ______ into the _____ cells so that's how you propagate mutations in tumor cells normally tumor cell should be pushed into apoptosis and it does everything it can to block it i.e. overexpressing ______2 which blocks release of ______ __ from _______ |
p53 g1 mutations daughters bcl2 cytochrome c mitochondria |
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other tumors do it by _______ p53 so that you can't get the apoptotic responses |
deleting/inactivating |
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in some colon cancers entire gene is ______ and in others _______ p53 is a ______ ______ gene and for these you have to delete or inactivate them (opp. of porto-oncogene to activate oncogene- this is opp. because job is to SLOW growth) |
deleted mutated tumor suppressor |
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distinction between oncogene and TSG
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oncogene is activated to give a tumor TSG's function is inactivated or deleted |
