Access
To read this article in full you may need to log in, make a payment or gain access through a site license (see right).
Letter
Nature Genetics 36, 877–882 (1 August 2004) | doi:10.1038/ng1389
Essential role of limiting telomeres in the pathogenesis of Werner syndrome
&
Abstract
Mutational inactivation of the gene WRN causes Werner syndrome, an autosomal recessive disease characterized by premature aging, elevated genomic instability and increased cancer incidence. The capacity of enforced telomerase expression to rescue premature senescence of cultured cells from individuals with Werner syndrome and the lack of a disease phenotype in Wrn-deficient mice with long telomeres implicate telomere attrition in the pathogenesis of Werner syndrome.
To read this article in full you may need to log in, make a payment or gain access through a site license (see right).
