Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of P27Kip1

Hiroaki Kiyokawa, Rhonda D. Kineman, Katia O. Manova-Todorova, Vera C. Soares, Eric S. Huffman, Masao Ono, Dilruba Khanam, Adrian C. Hayday, Lawrence A. Frohman, Andrew Koff

Research output: Contribution to journalArticlepeer-review

1109 Citations (Scopus)

Abstract

Disruption of the cyclin-dependent kinase-inhibitory domain of p27 enhances growth of mice. Growth is attributed to an increase in cell number, due to increased cell proliferation, most obviously in tissues that ordinarily express p27 at the highest levels. Disruption of p27 function leads to nodular hyperplasia in the intermediate lobe of the pituitary. However, increased growth occurs without an increase in the amounts of either growth hormone or IGF-I. In addition, female mice were infertile. Luteal cell differentiation is impaired, and a disordered estrus cycle is detected. These results reflect a disturbance of the hypothalamic-pituitary-ovarian axis. The phenotypes of these mice suggest that loss of p27 causes an alteration in cell proliferation that can lead to specific endocrine dysfunction.

Original languageEnglish
Pages (from-to)721-732
Number of pages12
JournalCell
Volume85
Issue number5
DOIs
Publication statusPublished - 1996 May 31

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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