Mice Lacking p27Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors

Keiko Nakayama, Noriko Ishida, Michiko Shirane, Akira Inomata, Tomoaki Inoue, Nobuyuki Shishido, Ikuo Horii, Dennis Y. Loh, Kei Ichi Nakayama

研究成果: Article査読

1455 被引用数 (Scopus)

抄録

Mice lacking p27Kip1 have been created by gene targeting in embryonic stem cells. These mice are larger than the control animals, with thymus, pituitary, and adrenal glands and gonadal organs exhibiting striking enlargement. CDK2 activity is elevated about 10-fold in p27-/- thymocytes. Development of ovarian follicles seems to be impaired, resulting in female sterility. Similarto mice with the Rb mutation, the p27-/- mice often develop pituitary tumors spontaneously. The retinas of the mutant mice show a disturbed organization of the normal cellular layer pattern. These findings indicate that p27Kip1 acts to regulate the growth of a variety of cells. Unexpectedly, the cell cycle arrest mediated by TGFβ, rapamycin, or contact inhibition remained intact in p27-/- cells, suggesting that p27Kip1 is not required in these pathways.

本文言語English
ページ(範囲)707-720
ページ数14
ジャーナルCell
85
5
DOI
出版ステータスPublished - 1996 5月 31
外部発表はい

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)

フィンガープリント

「Mice Lacking p27Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル