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Arachidonic acid is the precursor to.. |
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COX enzymes (cyclooxygenase) |
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cyclic endoperoxides such as the prostaglandins and thromboxanes |
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Required to Initiate Cell Cycle |
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Phosphorylate key proteins |
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G1-CdK and G1/S-CdK lead to |
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S-phase & activation of S-CdK |
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transition through M phase |
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Increased activity of G1-CdK and G1/S-CdK |
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release of E2F & entry into S phase |
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a transcription factor that increases expression of proteins needed for S-phase |
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G1-CdK and G1/S-CdK phosphorylate |
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How does activation of G1-CDK and G1/S-CDK lead to activation of S-CDK and entry into S phase? |
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G1-CdK and G1/S-CdK phosphorylate Rb. Rb leads to release E2F, and E2F pushes to S phase |
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How is G1-CDK and G1/S-CDK activated from mitogen binding? |
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Mitogen binding leads to stimulation of Ras/MAPK pathway. MAPK activates a gene regulatory protein (transcription factor), which increases myc. Myc regulates Cyclin D, SCF, and E2F. Cyclin D expression leads to the activation of G1-CDK, SCF degrades p27 which will lead to more G1/S-CdK, E2F pushes to S phase |
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How does the cell prevent entry into S phase if there is DNA damage? |
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DNA damage leads to activation of a kinsase (ATM or ATR) which then phosphorylates p53. p53 increases p21, p21 binds to G1/S-CdK and S-CdK inhibiting their activity |
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ubiquinates (degrades) p53 |
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binds to G1/S-CdK and S-CdK inhibiting their activity |
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phosphorylate M-CDK (CAK = activating phosphate, Wee1 = inhibitory phosphase) |
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binds to M-CDK forming the M-CDK complex |
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removes the inhibitory phosphate that Wee1 added to activate M-CdK |
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most events in M phase, such as APC activation and chromosomal segregation |
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inhibits activation of G1/S-CDK |
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degrades p27, so increase of G1/SCdK |
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kinases that phosphorylate p53 so mdm2 will stay bound and keep degrading p53 |
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E2F, p53, myc, unnamed that MAPK activate |
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SCF (ubiquinates p27), mdm2 (ubiquinates p53), APC (ubiquinates securin |
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pulls the sister chromatids apart |
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