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Hi, can you elaborate about the following: certain characterize mutations in p63 and compare that to known mutations in p53.
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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.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?List the regulatory mechanisms that might be lost in a cell producing faulty p53.
- Equalizing the Expression of X Chromosome Genes in Males and Females Males have only one X chromosome and therefore only one copy of all genes on the X chromosome. Each gene is directly expressed, thus providing the basis of hemizygosity in males. Females have two X chromosomes, but one is always inactivated. Therefore, females, like males, have only one functional copy of all the genes on the X chromosome. Again, each gene must be directly expressed. Why, then, are females not considered hemizygous, and why are they not afflicted with sex-linked recessive diseases as often as males are?A mutated gene that codes for an altered version of Cdk that is active in the absence of cyclin is a(n) ___________ . kinase inhibitor tumor suppressor gene proto-oncogene oncogene.Do cells which lack normal cell cycle control (cancerous cells) exhibit karyotypes that look physically different than cells with normal cell cycle control?
- Explain the concept of loss of heterozygosity (LOH). Why do most cancer cells exhibit LOH of one or more genes? How does failure of the spindle assembly checkpoint lead to loss of heterozygosity?What might explain the association between malignant tumors and chromosomal abnormalities? What's the difference between cancer cells and normal cells? Consider cell cycle checkpoints, density dependency, anchorage-dependency, and growth hormones like PDGFDescribe the nature of p53 reactivation as acancer-fighting strategy
- #9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.Hi, can you explain this concept: cell cycle progression can be halted at several points by the tumor suppressor gene product p53, activated in response to checkpoints sensing DNA and possibly also chromosome damage; loss of p53 would remove this brake to cycling. How these events can lead to cancer progression?Define about Several types of cellular stress events bring about rapidincreases in the nuclear levels of activated p53 protein ?
