Werner syndrome and the function of the Werner protein; what they can teach us about the molecular aging process.
Author(s) -
Patricia L. Opresko,
WenHsing Cheng,
Cayetano von Kobbe,
Jeanine A. Harrigan,
Vilhelm A. Bohr
Publication year - 2003
Publication title -
carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.688
H-Index - 204
eISSN - 1460-2180
pISSN - 0143-3334
DOI - 10.1093/carcin/bgg034
Subject(s) - werner syndrome , genome instability , premature aging , progeria , dna repair , chromosome instability , disease , cataracts , cancer , biology , senescence , accelerated aging , genetics , medicine , dna damage , gerontology , dna , bioinformatics , gene , chromosome , chemistry , helicase , rna
Werner syndrome (WS) is a hallmark premature aging disease, in which the patients appear much older than their chronological age, and exhibit many of the clinical signs and symptoms of normal aging at an early stage in life. They develop many age-associated diseases early in life including atherosclerosis, osteoporosis, cataracts and display a high incidence of cancer. WS is also marked by increased genomic instability, manifested as chromosomal alterations. Characterization and study of the Werner protein (WRN) suggests that it participates in several important DNA metabolic pathways, and that its primary function may be in DNA repair processes. Thus, the WRN protein represents an important link between defective DNA repair and the processes related to aging and cancer.
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