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- Define Explain the role of CDK inhibitors. If cyclin-CDK com-plexes are necessary to allow regulated progression through the eukaryotic cell cycle, what would be the physiologicalrationale for CDK inhibitors?During M phase of the cell cycle, how M-Cdk can trigger cohesin dissociation?Explain the role of CDK inhibitors. If cyclin-CDK complexes are necessary to allow regulated progression through the eukaryotic cell cycle, what would be the physiological rationale for CDK inhibitors?
- List the regulatory mechanisms that might be lost in a cell producing faulty p53.Figure 28.11 depicts the eukaryotic cell cycle. Many cell types “exit� the cell cycle and don’t divide for prolonged periods, a state termedG0; some, for example neurons, never divide again. a. In what stage of the cell cycle do you suppose a cell might be when it exits the cell cycle and enters G0? b. The cell cycle is controlled by checkpoints, cyclins, and CDKs. Describe how biochemical events involving cyclins and CDKs might control passage of a dividing cell through the cell cycle.The destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?
- in term of signal transduction how cell cycle/division is controlled?? ((while you are answerig plz write the refrence.))Cancer cells typically lose cell cycle entry control. Explain how the following mutations, which are found in some cancer cells, lead to a bypass of these controls: (a) overexpression of cyclin D, (b) loss of Rb function, (c) loss of p16 function, (d) hyperactive E2F.# 3 You've engineered a mutant cell where the FADD adapter was truncated. The mutant FADD only contains the Death Domain, and lacks the Death Effector Domain. What is the most likely phenotypic outcome for this mutant cell when presented with the Fas ligand? 20 E O The Fas/FasL oligomer is formed, but apoptosis is blocked O The Fas/FasL oligomer is formed, and apoptosis is hyperactivated O The Fas/FasL oligomer is not formed, and apoptosis is blocked O The Fas/FasL oligomer is not formed, but apoptosis is hyperactivated F3 $ 4 DOD 000 R F4 % 5 F5 T BARAT 6 tv @ MacBook Air F6 Y & 7 F7 U * ➤11 8 F8 · 9 F9
- Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.The expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.GAP protien mutation from Arg 789 to alanine constituvely activate the MAPK pathway by preventing GTPase activity of RAS protein. Is this affecting G2 check point cell cycle? If then, how?
