Antagonistic pleiotropy, mutation accumulation, and human genetic disease
dc.contributor.author | Albin, Roger L. | en_US |
dc.date.accessioned | 2006-09-08T20:44:17Z | |
dc.date.available | 2006-09-08T20:44:17Z | |
dc.date.issued | 1993-02 | en_US |
dc.identifier.citation | Albin, Roger L.; (1993). "Antagonistic pleiotropy, mutation accumulation, and human genetic disease." Genetica 91 (1-3): 279-286. <http://hdl.handle.net/2027.42/42801> | en_US |
dc.identifier.issn | 0016-6707 | en_US |
dc.identifier.issn | 1573-6857 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/42801 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8125276&dopt=citation | en_US |
dc.description.abstract | The antagonistic pleiotropy theory of senescence is the most convincing theoretical explanation of the existence of aging. As yet, no locus or allele has been identified in a wild population with the features predicted by the pleiotropic theory. Human genetic diseases offer the opportunity to identify potentially pleiotropic alleles/loci. Four human genetic diseases—Huntington's disease, idiopathic hemochromatosis, myotonic dystrophy, and Alzheimer's disease—may exhibit pleiotropic effects and further study of these diseases might result in the identification of pleiotropic genes causing aging. Inability to find an early life selective benefit associated with these disease-causing alleles would favor the major alternative genetic explanation for aging, the mutation accumulation theory. | en_US |
dc.format.extent | 799095 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers; Springer Science+Business Media | en_US |
dc.subject.other | Life Sciences | en_US |
dc.subject.other | Human Genetics | en_US |
dc.subject.other | Microbial Genetics and Genomics | en_US |
dc.subject.other | Plant Genetics & Genomics | en_US |
dc.subject.other | Animal Genetics and Genomics | en_US |
dc.subject.other | Aging | en_US |
dc.subject.other | Huntington's Disease | en_US |
dc.subject.other | Hemochromatosis | en_US |
dc.subject.other | Myotonic Dystrophy | en_US |
dc.subject.other | Alzheimer's Disease | en_US |
dc.title | Antagonistic pleiotropy, mutation accumulation, and human genetic disease | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Ecology and Evolutionary Biology | en_US |
dc.subject.hlbsecondlevel | Natural Resources and Environment | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Neurology, University of Michigan, 48109, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 8125276 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/42801/1/10709_2005_Article_BF01436004.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF01436004 | en_US |
dc.identifier.source | Genetica | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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