Regulation of BRCA1 Function by Physophorylation.

Abstract

The purpose of the studies outlined herein was to map phosphorylation sites on the BRCA1 protein as well as study the effects of these modifications on BRCA1 function. In numerous metabolic labeling studies, it has proven impossible to incorporate sufficient 32-Phosphate into the protein to properly carry out phosphopeptide mapping studies. In order to determine the mechanism of aberrant subcellular localization of BRCA1 in breast cancer, a series of deletion mutants of the protein, all containing the nuclear localization sequences, were prepared as green fluorescent protein fusions, expressed in both normal and transformed human breast cell lines and identified by fluorescence microscopy. The results indicate that the amino terminus of the protein may contain a motif that must be modified before the protein translocates from the cytoplasm to the nucleus. The development of a BRCA1 somatic cell knockout breast epithelial cell line through targeted disruption was begun. Screening of 100 drug resistant colonies generated one homologously targeted clone. Unfortunately, screening of several hundred clones in a second round of targeting failed to detect targeting of the second allele, indicating that BRCA1 expression is required for survival in cell culture, at least in the cell line being targeted.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 1998
Accession Number
ADA364735

Entities

People

  • Michael T. Furlong

Organizations

  • University of Texas Health Science Center at San Antonio

Tags

DTIC Thesaurus Topics

  • Biomedical And Dental Materials
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Cytoplasm
  • Epithelial Cells
  • Materials
  • Medical Personnel
  • Neoplasms
  • Peptides
  • Phosphorylation
  • Polymeric Films
  • Proteins
  • Targeting
  • Transcription Factors

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Molecular Genetics
  • Molecular and genetic basis of cancer.