Roles of the Werner syndrome RecQ helicase in DNA replication

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Roles of the Werner syndrome RecQ helicase in DNA replication.

Congenital deficiency in the WRN protein, a member of the human RecQ helicase family, gives rise to Werner syndrome, a genetic instability and cancer predisposition disorder with features of premature aging. Cellular roles of WRN are not fully elucidated. WRN has been implicated in telomere maintenance, homologous recombination, DNA repair, and other processes. Here I review the available data ...

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Functional role of the Werner syndrome RecQ helicase in human fibroblasts.

Werner syndrome is an autosomal recessive human genetic instability and cancer predisposition syndrome that also has features of premature aging. We focused on two questions related to Werner syndrome protein (WRN) function in human fibroblasts: Do WRN-deficient fibroblasts have a consistent cellular phenotype? What role does WRN play in the recovery from replication arrest? We identified consi...

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Divergent cellular phenotypes of human and mouse cells lacking the Werner syndrome RecQ helicase.

Werner syndrome (WS) is a human autosomal recessive genetic instability and cancer predisposition syndrome with features of premature aging. Several genetically determined mouse models of WS have been generated, however, none develops features of premature aging or an elevated risk of neoplasia unless additional genetic perturbations are introduced. In order to determine whether differences in ...

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The effect of 2-deoxy-D-glucose on Werner syndrome RecQ helicase gene.

Caloric restriction (CR) is known to effectively elongate mammalian life-spans. The compound 2-deoxy-D-glucose (2DG), which is often used as an inhibitor of glucose utilization, is a mimetic agent of CR. In this study, we examined the changes of telomerase and Werner's syndrome RecQ (WRN) helicase after treatment with 2DG, because of the involvement of recQ helicase in the regulation of telomer...

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ژورنال

عنوان ژورنال: DNA Repair

سال: 2008

ISSN: 1568-7864

DOI: 10.1016/j.dnarep.2008.07.017