Elucidating cdc25's Oncogenic Mechanism in Breast Cancer Using Pin1, a Negative Mitotic Regulator

Abstract

The current study demonstrates that Pin1 functions in the control of the G2/M transition in Xenopus laevis egg extracts. We show that extracts depleted of Pin1 protein enter mitosis prematurely, a phenotype which is dramatically potentiated under circumstances in which the replication checkpoint has been triggered. The replication checkpoint functions as a failsafe mechanism which enables the postponement of the entry into mitosis in response to unreplicated DNA; in this system the extent of the delay correlates with the amount of chromatin added to the extract. Extracts from which Pin1 has been quantitatively depleted undergo the G2/M transition with rapid kinetics regardless of DNA concentration, while control extracts display a robust checkpoint response triggered by the presence of unreplicated DNA.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 1999
Accession Number
ADB258830

Entities

People

  • Katharine E. Winkler

Organizations

  • Duke University Hospital

Tags

DTIC Thesaurus Topics

  • Abstracts
  • Biomedical Research
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chromosome Structures
  • Dynamics
  • Enzyme Inhibitors
  • Fungi
  • Genetic Structures
  • Genetics
  • Genome
  • Governments
  • Neoplasms
  • Regulators
  • Transitions

Readers

  • Immunology
  • Molecular Biology and Genetics