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Name four downstream effects of p53 activation.
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- What must occur for TP53 to no longer function properly?List the regulatory mechanisms that might be lost in a cell producing faulty p53.The p53 pathway is important for regulating the cell cycle. In a normal cell, there is a protein called mdm2 that can bind to p53 and deactivate it. A diseased individual has amutation in the gene that codes for mdm2, resulting in an mdm2 protein that is less able to bind to p53. Will this mutation increase, decrease, or cause no change in the rate of cell death? Explain.
- What is the rationale for synthesizing and rapidly degrading p53 protein in the cell?Li- Fraumeni Syndrome (LFS) is a rare hereditary cancer disease due to a mutation in the TP53 gene. Propose a treatment strategy for LFS.Why is it advantageous for p53 to be activated by factors such as ER stress, light, and hypoxia (low oxygen concentration)?
- What role does p53 signaling play in normal cells?Individuals with the hereditary disorder ataxia telangiectasia suffer from neurodegeneration, immunodeficiency, and an increased incidence of cancer. The genetic basis for ataxia telangiectasia is a loss-of-function mutation in the gene encoding ATM (ATM; ataxia telangiectasia mutated). Besides p53, what other substrate is phosphorylated by ATM? How does the phosphorylation of this substrate lead to inactivation of CDKs to enforce cell cycle arrest?If you were to design an experiment to get p53 back into cancer cells, how would you go about that work? How would you direct p53 into the nucleus of cancer cells without directing it to the nucleus of healthy cells? As an overabundance of p53 in healthy cells would cause problems. Could someone in depth answer these questions for me and explain them cellularly.
- Identify and list the functions of the three general classes of proteins that control cell death.Briefly discuss somatic hypermutation. What is the function of SH? What does SH result in? Name the enzyme that catalyzes SH.Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.