Telomeres, hidden mosaicism, loss of heterozygosity, and complex genetic traits

被引:17
作者
Aviv, A
Aviv, H
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Hypertens Res Ctr, Newark, NJ 07103 USA
[2] Univ Med & Dent New Jersey, New Jersey Med Sch, Cytogenet Lab, Ctr Human & Mol Genet, Newark, NJ 07103 USA
关键词
D O I
10.1007/s004390050774
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Telomeres appear to function as an endogenous timing mechanism in human beings. Telomere attrition not only provides a satisfactory explanation for some aspects of aging, it might also resolve enigmatic features of complex genetic traits that are age-dependent. If, with the passage of time, telomere attrition in human beings leads to genomic instability and particularly the loss of chromosomes, then the ase dependency of phenotypic expressions of complex genetic traits might result from the temporal loss of heterozygosity and the consequent expression of disease-causing genes. In this way, telomere attrition might play a role not only in aging, but also in the diverse expression of complex genetic traits, such as essential hypertension, non-insulin-dependent diabetes mellitus, atherosclerosis, and cancer.
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页码:2 / 4
页数:3
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