Werner Syndrome Essay Research Paper AbstractNowadays those — страница 4

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determinants of aging in animals remain unknown. In addition, using yeast as a model for human aging in general may give insight into the mechanisms of Werner syndrome and related diseases. A yeast protein similar to the human WRN protein, called SGS1, has been found. Mutations in SGS1 cause yeast to have a shorter lifespan than yeast cells without the mutation, and shown other signs typical of aging in yeast, such as an enlarged and fragmented nucleolus. It is not even understood whether aging is determined by organism-wide processes, such as hormonal changes, or by events occurring individually in different cells, tissues, or organs. Only with the experimental flexibility provided by an animal model would it be possible to establish whether accelerated aging actually occurs in

Werner syndrome and how this aging occurs. Conclusion: The function of the Werner syndrome helicase is currently unknown. What is clear is that subjects with the syndrome probably do not produce a functional form of this protein. It is known that DNA in affected subjects appears to contain a large number of damaged sites. This accumulation of DNA damage is probably the cause of the symptoms we call Werner syndrome. Cells from Werner syndrome subjects do not appear to be defective for any known DNA repair process, so the primary defect probably involves a defect in a process that causes DNA damage, rather than one that repairs damage caused by other agents. Whatever the specific mechanisms involved in the Werner syndrome phenotype, identification of the Werner syndrome gene now

provides evidence that at least some components of normal aging and disease susceptibility in late life may be related to disfunctions in DNA metabolism. Fortunately, we have the responsible gene in hand, giving a tool to begin answering all of these puzzling questions. The Aging Gene Discovered: Werner Syndrome Homozygous germ cells oncogenes phenotype Bibliography Annotated Bibliography Adoue, Daniel. Werner’s Syndrome. New England Journal of Medicine vol 337. 1997. This is a shocking picture of someone diagnosed with Werner’s syndrome. It is a good picture to understand exactly what this syndrome does to a persons body. This 38 year old man looks as if he is much older. Bauer, Eugene A. “Diminished Response of Werner’s Syndrome Fibroblasts to Growth Factors PDGF and

FGF”. Science, vol 234: 1240-1244, 1996. Patient’s with Werner’s syndrome, undergo an accelerated aging process that leads to premature death. Fivroblasts from such patients typically grow poorly in culture. Here it is shown that fibroblasts from a patient with Werner’s syndrome have a markedly attenuated mitogenic response to platelet-derived growth factor and fibroblast growth factor. Goto, Makoto.; Rubenstein, Mark. “Genetic linkage of Werner’s syndrome to five markers on chromosome 8″. Nature v. 355. 1992. This is an article about progeria and it’s linkage to familial diseases. It is also about the linkage found of werner’s syndrome to certain markers on a chromosomes. Khraishi, M.; Howard, B. A patient with Werner’s syndrome and osteosarcoma presenting as

scleroderma. J. Rheum. 19: 810-813, 1992. This is an article about a specific case of a person with both Werner’s syndrome and osteosarcoma. It describes the case and gives some examples of the early onset problems that they had. Martin, George. ” What do we know about the cause of Werner Syndrome and progeria, the disease that leads to premature aging in children”. Scientific American. University of Washington, 1992. This article asks many scientists questions about Werner’s syndrome. In addition, it contrasts Werner’s syndrome and Hutchinson-Gilford syndrome giving many different scientific opinions on both syndromes. Morozov, Vladimir; Mushegian, Arcady. “A putative nucleic acid-binding domain in Bloom’s and Werner’s syndrome helicases”. Trends in Biochemical

Sciences v. 22. United Kingdom, 1997. The identification of a putative necleic acid-binding domain in Bloom’s and Werner’s syndrome helicases is reported. These disorders are associated with a notable predisposition to various cancers, and the proteins involved are both very similar to helicases of the RecQ family. Moser, Michael. “WRN mutations in Werner Syndrome”. University of Washington, Seattle: 1998. Werner syndrome is one of a group of human genetic diseases that have recently been linked to deficits in cellular helicase function. This is a review of the spectrum of WS-associated WRN mutations, the organization and potential functions of the WRN protein, and potential mechanistic links between the loss of the WRN function and pathogenesis of the WS clinical and