what are the rolls that the p53 gene and RAS protein take on when trying to stop a cancer cell from further replicating. Also, what would happen if a mutation were to occur in both genes
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what are the rolls that the p53 gene and RAS protein take on when trying to stop a cancer cell from further replicating. Also, what would happen if a mutation were to occur in both genes?
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- Do you think there are more unique alleles of p53 that lead to cancer or more unique alleles of Ras that lead to cancer? Please explain.D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…Part of the Ras protein is associated with the plasma membrane, and part extends into the cytoplasm. How does the Ras protein transmit a signal from outside the cell into the cytoplasm? What happens in cases where the ras gene is mutated?
- We have studied Ras signal transduction pathway. In an experiment, two different mutations were produced using different chemicals. The proteins with mutation are listed below. State what will be the effect of each mutation and explain whether it will result in cell proliferation or not. GEF protein GTPaseDistinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.You are interested in studying a novel gene that appears to be involved in cancer. There is no information about the function of this gene. What would you do to obtain the cDNA for this gene? How would you express this gene and what expression systems might you utilize to study its function and why? How would determine the subcellular localization of this gene in eukaryotic cells? What are alternative methods in case one doesn't work? How would you purify and determine the 3-dimensional structure of this protein?
- D) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressedOur understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation.
- According to the multi-hit model, more than one mutation must occur in a cell for cancer to develop. Once an oncogene has been formed by a mutation, what other type of gene must also mutate?p53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?Our understanding of the molecular biology of cancer formation has been greatly enhanced by studying oncogenic viruses. Answer the following questions regarding oncogenic retroviruses? What is an oncogene? How does if differ from a proto-oncogene? Why are retroviruses prone to accumulating oncogenes? Explain how a gain of function mutation in the Ras protein caused by a retrovirus might lead to cancer formation