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18 Cards in this Set
- Front
- Back
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mitogens |
promote mitosis |
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Explain path from mitogen to cell cycle activation |
mitogen activates G1-cdk-> phosphorylate Rb and E2F -> Rb and E2F detatch-> inactivate R-> E2F activated-> E2F activates cell cycle |
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Myc |
TF, leads to active G1-Cdk |
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Rb pathway |
mitogen+ mitogen receptor-> Ras (GDP)-> Ras GTP-> MAP3K-> MAP 2K-> MAPK-> Myc activation-> activate G1-cdk-> phosphorylate (Rb+ E2F)-> Disassociate-> E2F induce expression of genes to enter cell cycle |
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TOR pathway |
growth factor—> binds to activated growth factor receptor-> PI3K activated-> PIP3 -> TOR activation-> induce increased ribosome production and protein synthesis-> cell growth |
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Extrinsic pathway |
Fas + Fas receptor-> DISC activated-> activate caspace-> ICAD and CAD separate-> CAD activate-> cleaves DNA |
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Extrinsic pathway |
Fas + Fas receptor-> DISC activated-> activate caspace-> ICAD and CAD separate-> CAD activate-> cleaves DNA |
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Intrinsic pathway |
P21-> induces increase in Bax/Bac -> Cytochrome C leaves mitochondria-> Apaf 1 activated-> apoptosome-> Caspace activated -> ICAD AND CAD separate-> CAD cleaves Dna |
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Proapoptosis |
Bac/Bax |
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Proapoptosis |
Bac/Bax |
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Anti-apoptotic |
Bcl2 |
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BCl2 Survival factors pathway |
survival factor (ligand) binds to receptor-> activate-> Activated TF-> goes to Nuc. -> Bcl2 protein made-> inhibits/ blocks apoptosis |
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What happens if Fas mutations? |
Autoimmune lymphoproliferative syndrome (ALPS) |
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What is ALPS? |
LOF, because cells dont end up dying |
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What does over expression of Bcl2 lead to ? |
B cell lymphomas, oncogene |
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Loss of function of Bcl2 |
apoptosis |
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Bax/ Bac not functioning= |
LOF, tumor suppressor |
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If anti apoptosis signals are too strong resulting in cancer, is there something we can do to lessen that signal? |
Drug that inhibits Bcl2 |
