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What is the rationale for synthesizing and rapidly degrading p53 protein in the cell?
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- p53 is a gene / protein often associated with cancer. Why? What does p53 do? What kind of gene is it? Is it associated more with any one particular type of cancer or all cancers? Tell me more about p53, but please do not exceed one typed page.How does p53 induce apoptosis? How does the cell determine what "too much" damage is? Meaning, how can it tell if the damage to the DNA is too severe to fix in order for the cell to move on to S phase? Thank you.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.
- My question is two fold. What are some diseases that cause and/or are caused by apoptosis? Also if apoptosis is the most common form of programmed cell death in animals, what other forms of programmed cell death are there? Thank you.What is the significance of the cell cycle control system and checkpoints? Explain step by step in your own words. [please make it simple]Name four downstream effects of p53 activation.
- Can you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below? In addition to phosphorylation, the C-terminal domain of p53 can also be acetylated and sumolated in response to DNA damage. Acetylation and sumolation both result in an increase in the transactivation ability of p53 and may account for this finding. In vivo, IR induces the acetylation of p53 at Lys320 by PCAF and Lys382 by CBP/p300. Acetylation at these sites is dependent on N-terminal phosphorylation at Ser15 and to a lesser extent on phosphorylation at Ser6, Ser9, and Thr18 (Saito et al., 2002; Wahl and Carr, 2001). All of these phosphorylation events are ATM-dependent, although only Ser15 has been shown to be phosphorylated directly by ATM. Sumolation occurs at Lys386 after DNA damage (Muller et al., 2000). Sumolation refers to the covalent attachment of a small ubiquitin-like molecule (SUMO-1) to Lys residues, but in contrast to ubiquitination, does not result…Can you think of two ways in which the function of p53 can be disrupted?Why are the proteins called p53 and Ras studied so much these days?
- You are working in a cell biology lab that investigates non-small cell lung cancer cells, which of these cellular features will be suggestive of senescence in the cells observed? Choose all that apply: Group of answer choices Large flattened morphology Reduced incorporation of 5-bromodeoxyuridine (in DNA replication) Increased p53 expression Decreased expression of p15INK4B. Please explain the role of Ubiquitin Ligase Activity in the regulation of apoptotic cell death.Which of the following would most likely promote necrosis? Select one: a. activation of p53 b. activation of cdk c. pathogenic infection d. inactivation of p53 e. cyclin Clear my choice