Cells deleted for Brca2 COOH terminus exhibit hypersensitivity to γ- radiation and premature senescence

M. Morimatsu, G. Donoho, Edward P Hasty

Research output: Contribution to journalArticle

99 Citations (Scopus)

Abstract

The putative Brca2-MmRad51 interaction is analyzed in mouse cells deleted for the COOH terminus of Brca2 (amino acids 3140-3328), which contains a region that associates with MmRad51 by yeast two-hybrid. These cells are hypersensitive to γ-radiation (suggesting defective recombinational repair) but not UV light (suggesting intact nucleotide excision repair) and maintain the G1-S and G2-M checkpoints after exposure to γ-irradiation. Cells deleted for the COOH terminus of Brca2 progress through the cell cycle at a similar rate as wild-type cells but undergo senescence more rapidly. These data support the hypothesis that deletion of Brca2 stimulates cancer by defective MmRad51-mediated DNA repair and not by defective cell cycle regulation.

Original languageEnglish (US)
Pages (from-to)3441-3447
Number of pages7
JournalCancer Research
Volume58
Issue number15
StatePublished - Aug 1 1998
Externally publishedYes

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Hypersensitivity
Radiation
DNA Repair
Cell Cycle
Cell Aging
Ultraviolet Rays
Yeasts
Amino Acids
Neoplasms

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Cells deleted for Brca2 COOH terminus exhibit hypersensitivity to γ- radiation and premature senescence. / Morimatsu, M.; Donoho, G.; Hasty, Edward P.

In: Cancer Research, Vol. 58, No. 15, 01.08.1998, p. 3441-3447.

Research output: Contribution to journalArticle

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