Prolactin signaling and Stat5: going their own separate ways?

被引：6

作者：

Brisken, C

Ayyanan, A

Doppler, W

机构：

[1] Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland

[2] Univ Innsbruck, A-6020 Innsbruck, Austria

来源：

BREAST CANCER RESEARCH | 2002年 / 4卷 / 06期

关键词：

cell adhesion; mammary epithelium; prolactin receptor; Stat5; steroid hormones;

D O I：

10.1186/bcr543

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Miyoshi et al. compared the role of the prolactin receptor (PrlR) and its downstream mediator, the signal transducer and activator of transcription 5 (Stat5), in mammary epithelial cells in vivo by studying PrlR(-/-) and Stat5ab(-/-) mouse mammary epithelial transplants during pregnancy. At first glance, the two mutant epithelia appear to have similar defects in the differentiation of the alveolar epithelium. However, a closer examination by Miyoshi et al. revealed defects in the epithelial architecture of the smallest ducts of Stat5ab(-/-) transplants not apparent in the PrlR(-/-) transplants, suggesting that Stat5 is more than a simple mediator of PrlR action.

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收藏

页码：209 / 212

页数：4

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