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In tumor cells Rb protein is hyperphosphorylated. In response to that, will p53 level increase or decrease? Why or why not?
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- In tumor cells Rb protein is hyperphosphorylated. In response to that, will p53 level increase or decrease? Why or why not?A cell begins to undergo apoptosis due to stress. Which of the following are true about this cell? (select all that apply) The cell can exit apoptosis if the stressful factor is removed The cell has high levels of p53. The cell's DNA will inevitably degrade The cell may undergo mitosis before completing apoptosiswe read that in tumor cells Rb protein is hyperphosphorylated. In response to that, will p53 level increase or decrease? Why or why not? I need new answers please
- 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.Normal p53 is a tumor suppressor gene, when mutated it loses this function. Explain how a tissue expressing normal p53 would lose control and have over-proliferation of the cells based on p53 levels.Determine if the gene on the left is a proto-oncogene or tumor suppressor. APC p53 Ras [Choose] [Choose] Tumor suppressor Proto-oncogene [Choose]
- 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.Why is the p53-meditated apoptosis pathway, and the GSK3 signaling pathway important for cancer therapy. Explain each of them in 3-5 sentences.Improper cell signaling can lead to cancer. True False
- // Which CDK and cyclin does p53 ultimately target in DNA damaged conditions? O CDK1/cyclin E O CDK2/cyclin E CDK1/cyclin B CDK2/cyclin BMatch the factor on the left with what it promotes on the right Mitogen Morphogen Death ligand [Choose] [Choose] Extrinsic Apoptosis Intrinsic Apoptosis Cell Survival Proliferation Differentiation TCHOUSET <Which of the following would result in cell cycle arrest? O phosphorylation of Rb by G1-Cdk phosphorylation of p53 O phosphorylation of helicase by S-Cdk phosphorylation of M-Cdk by CAK phosphorylation of APC by M-Cdk
