Loss of transcription factor IRF-1 affects tumor susceptibility in mice carrying the Ha-ras transgene or nullizygosity for p53

被引：118

作者：

Nozawa, H

Oda, E

Nakao, K

Ishihara, M

Ueda, S

Yokochi, T

Ogasawara, K

Nakatsuru, Y

Shimizu, S

Ohira, Y

Hioki, K

Aizawa, S

Ishikawa, T

Katsuki, M

Muto, T

Taniguchi, T

Tanaka, N ^{[1
]}

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Immunol, Tokyo 1130033, Japan

[2] Univ Tokyo, Grad Sch Med, Dept Surg Oncol, Tokyo 1130033, Japan

[3] Univ Tokyo, Grad Sch Med, Dept Pathol, Tokyo 1130033, Japan

[4] Univ Tokyo, Fac Med, Tokyo 1130033, Japan

[5] Univ Tokyo, Dept Dna Biol & Embryo Engn, Inst Med Sci, Minato Ku, Tokyo 1088639, Japan

[6] Cent Inst Expt Anim, Miyamae Ku, Kawasaki, Kanagawa 2160001, Japan

[7] Kumamoto Univ, Fac Med, Inst Mol Embryol & Genet, Kumamoto 8600811, Japan

来源：

GENES & DEVELOPMENT | 1999年 / 13卷 / 10期

关键词：

IRF-1; c-Ha-ras; p53; tumor susceptibility gene; mutation frequency;

D O I：

10.1101/gad.13.10.1240

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The transcription factor IRE-I has been implicated in tumor suppression: IRF-1 suppresses cell transformation and mediates apoptosis in vitro. Here we show that the loss of IRF-1 alleles per se has no effect on spontaneous turner development in the mouse but dramatically exacerbates previous tumor predispositions caused by the c-Ha-ras transgene or by nullizygosity for p53. Grossly altered tumor spectrum, as compared to p53-null mice, was also observed in mice lacking both IRE-I and p53, and cells from these mice show significantly higher mutation rate. Our results suggest that IRF-1 is a new member of the tumor susceptibility genes.

引用

页码：1240 / 1245

页数：6

共 41 条

[1] Atm-deficient mice: A paradigm of ataxia telangiectasia [J].