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

Research output: Contribution to journalArticlepeer-review

1430 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)707-720
Number of pages14
JournalCell
Volume85
Issue number5
DOIs
Publication statusPublished - 1996 May 31
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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