Regulation of the Werner helicase through a direct interaction with a subunit of protein kinase A

Duy T. Nguyen, Ilsa I. Rovira, Toren Finkel

Research output: Contribution to journalArticle

Abstract

Werner syndrome is a hereditary disease characterized by cancer predisposition, genetic instability, and the premature appearance of features associated with normal aging. At the molecular level this syndrome has been related to mutations in the Werner helicase, a member of the RecQ family of DNA helicases which are required to maintain genomic stability in cells. Here we show by a yeast two-hybrid screen that the Werner helicase can directly interact with the regulatory subunit (RIβ) of cAMP protein kinase A (PKA). We confirm that this interaction occurs in vivo. Interestingly, serum withdrawal causes a redistribution of the Werner helicase within the nucleus of mammalian cells. Raising intracellular cAMP levels or increased expression of the regulatory but not the catalytic subunit of PKA inhibits this nuclear redistribution stimulated by serum deprivation. These results suggest that similar to lower organisms, gene products linked to genomic instability and aging may be directly regulated by growth factor-sensitive, PKA-dependent pathways.

Original languageEnglish (US)
Pages (from-to)170-174
Number of pages5
JournalFEBS Letters
Volume521
Issue number1-3
DOIs
StatePublished - Jun 19 2002
Externally publishedYes

Keywords

  • Aging
  • Helicases
  • RecQ
  • Signal transduction
  • Werner syndrome

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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