SH2-B is required for both male and female reproduction

被引：55

作者：

Ohtsuka, S

Takaki, S

Iseki, M

Miyoshi, K

Nakagata, N

Kataoka, Y

Yoshida, N

Takatsu, K

Yoshimura, A

机构：

[1] Kyushu Univ, Med Inst Bioregulat, Div Mol & Cellular Immunol, Higashi Ku, Fukuoka 8128582, Japan

[2] Kurume Univ, Inst Life Sci, Div Mol Genet, Kurume, Fukuoka 8390861, Japan

[3] Kumamoto Univ, Ctr Anim Res & Dev, Div Reprod Engn, Kumamoto 8600811, Japan

[4] Univ Tokyo, Inst Med Sci, Div Immunol, Dept Microbiol & Immunol,Minato Ku, Tokyo 1088639, Japan

[5] Univ Tokyo, Inst Med Sci, Lab Gene Express & Regulat, Ctr Med Expt,Minato Ku, Tokyo 1088639, Japan

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2002年 / 22卷 / 09期

关键词：

D O I：

10.1128/MCB.22.9.3066-3077.2002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Many growth factors and hormones modulate the reproductive status in mammals. Among these, insulin and insulin-like growth factor I (IGF-I) regulate the development of gonadal tissues. SH2-B has been shown to interact with insulin and IGF-I receptors, although the role of SH2-B in these signals has not been clarified. To investigate the role of SH2-B, we generated mice with a targeted disruption of the SH2-B gene. Both male and female SH2-B-/- mice showed slight retardation in growth and impaired fertility. Female knockout mice possess small, anovulatory ovaries with reduced numbers of follicles and male SH2-B-/- mice have small testes with a reduced number of sperm. SH2-B-/- cumulus cells do not respond to either follicle-stimulating hormone or IGF-I. These data suggest that SH2-B plays a critical role in the IGF-1-mediated reproductive pathway in mice.

引用

页码：3066 / 3077

页数：12

共 48 条

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