Changes to the p53 protein structure can be caused by differences in DNA and can affect protein function." Can you give detailed explanation why this is causation and not correlation? The explanation should be related with mutation, structure changes during protein synthesis, chemical property changes in amino acids, and functions of p53 protein.
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"Changes to the p53 protein structure can be caused by differences in DNA and can affect protein function."
Can you give detailed explanation why this is causation and not correlation?
The explanation should be related with mutation, structure changes during protein synthesis, chemical property changes in amino acids, and functions of p53 protein.
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- Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function. Hint: Loss of p53 function occurs in the majority of human tumors.: The effects of DNA mutations within the p53 gene on the structure and function of the protein encoded by the gene. The essay should focus on the following discussion points: The normal functions of the p53 gene. Known mutations of the gene. The impact of mutations on the structure of the protein encoded by the gene. The impact of mutations on the function of the protein. Current therapeutic interventions that aim to address the impact of mutations on gene functionLoss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.
- In a few sentences, describe how p53 guards the genome. Include at least two specific ways that p53 guards the genome. In a few more sentences, describe the structure and function of the p53 protein. Structure: what domains are present in the p53 protein? Do p53 work as a single protein or as part of a complex? Function: what do the different domains do? How can p53 do so many different things?Li- Fraumeni Syndrome (LFS) is a rare hereditary cancer disease due to a mutation in the TP53 gene. Propose a treatment strategy for LFS.Define a Point mutation and give an example. What is sickle cell anemia and what causes it. What is nondisjunction? How does nondisjunction cause disorders? NUMER YOUR ANSWERS
- A region on chromosome 6 has been linked to schizophrenia, but researchers have not found a specific gene associated with this disease. What steps would be necessary to locate the gene?Acquired mutation in the p53 gene is the most common genetic alteration found in human cancer (> 50% of all cancers). A germline mutation in p53 is the causative lesion of Li- Fraumeni familial cancer syndrome. In many tumors, one p53 allele on chromosome 17p is deleted and the other is mutated. What type of protein is encoded by the p53 gene? (A) Caspase (B) DNA repair enzyme (C) Membrane cell adhesion molecule (D) Serine phosphatase (E) Telomerase (F) Transcription factor (G) Tyrosine kinaseIndividuals 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?
- Find non-cancerous, non--nonsense, point mutation genetic disease. Describe the disease's name and the type of mutation. Compare the gene sequence between wild type and mutant. Compare the polypeptide sequence and structure encoded by the wild type's gene and the mutant's gene. Describe and explain the consequences of the mutation to a patient's health. Note: 1. These questions will test the concepts of DNA-Protein transcription and translation on the effects of mutation. 2. Using dissimilar example/solution from your classmate and lecture's notes is encouraged. 3. Provide citation and reference.Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed. Select the two mechanisms. Identify two genetic mechanisms whereby proto-oncogenes can become overexpressed.Select the two mechanisms. 1) alterations in chromatin structure 2) a gain-of-function alteration 3)modification of proto-oncogenes products 4)mutations that result in an abnormal protein product 5)mutations within gene-regulatory regionsThe P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.