Factors that Effect Signal Transduction by the Estrogen Receptor.

Abstract

This project examines the mechanism of signal transduction by the estrogen receptor (ER), a hormone dependent transcriptional regulator involved in many human breast tumors. We have found that ectopic expression of the cyclin A/cdk2 kinase complex increases hormone-dependent transcriptional activity by the estrogen receptor in vivo. This effect can be further enhanced by the concurrent expression of cyclin-dependent kinase activators, CAKs, and abolished by coexpression of the cdk inhibitor (CDI), p27. Likewise, ER-dependent transcriptional activation is reduced by the expression of a dominant negative cdk2 mutant in mammalian cells or by deletion of a potential cyclin A homologue, Clb4, in yeast. ER is also phosphorylated in vitro by cyclin A/cdk2 and incorporation of phosphate into ER is stimulated by the ectopic expression of cyclin A in vivo. Together, these results strongly suggest a role for cyclin-dependent kinases in the regulation of ER transcriptional enhancement.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 1995
Accession Number
ADA311359

Entities

People

  • Michael J. Garabadian

Organizations

  • NYU Langone Health

Tags

DTIC Thesaurus Topics

  • Breast Cancer
  • Carrier Proteins
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Epithelial Cells
  • Estrogens
  • Hormones
  • Inhibitors
  • Laboratory Animals
  • Materials
  • Neoplasms
  • New York
  • Phosphorylation
  • Proteins
  • Regulations
  • Regulators

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.