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

M. Morimatsu; G. Donoho; P. Hasty

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

M. Morimatsu
, G. Donoho
, P. Hasty

Research output: Contribution to journal › Article › peer-review

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 language	English (US)
Pages (from-to)	3441-3447
Number of pages	7
Journal	Cancer Research
Volume	58
Issue number	15
State	Published - Aug 1 1998
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

Cite this

@article{b3fd0f886b43497fac93d4c5a2802869,

title = "Cells deleted for Brca2 COOH terminus exhibit hypersensitivity to γ- radiation and premature senescence",

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.",

author = "M. Morimatsu and G. Donoho and P. Hasty",

year = "1998",

month = aug,

day = "1",

language = "English (US)",

volume = "58",

pages = "3441--3447",

journal = "Cancer Research",

issn = "0008-5472",

number = "15",

}

TY - JOUR

T1 - Cells deleted for Brca2 COOH terminus exhibit hypersensitivity to γ- radiation and premature senescence

AU - Morimatsu, M.

AU - Donoho, G.

AU - Hasty, P.

PY - 1998/8/1

Y1 - 1998/8/1

N2 - 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.

AB - 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.

UR - https://www.scopus.com/pages/publications/0032145477

UR - https://www.scopus.com/pages/publications/0032145477#tab=citedBy

M3 - Article

C2 - 9699678

AN - SCOPUS:0032145477

SN - 0008-5472

VL - 58

SP - 3441

EP - 3447

JO - Cancer Research

JF - Cancer Research

IS - 15

ER -

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

Abstract

ASJC Scopus subject areas

Other files and links

Fingerprint

Cite this