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: ジャーナルへの寄稿記事

1406 引用 (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.

元の言語英語
ページ(範囲)707-720
ページ数14
ジャーナルCell
85
発行部数5
DOI
出版物ステータス出版済み - 5 31 1996

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Retinal Dysplasia
Retinal Neoplasms
Thymus
Pituitary Neoplasms
Body Size
Sirolimus
Stem cells
Hyperplasia
Tumors
Animals
Genes
Display devices
Cells
Contact Inhibition
Female Infertility
Ovarian Follicle
Gene Targeting
Pituitary Gland
Thymocytes
Embryonic Stem Cells

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

これを引用

Mice Lacking p27Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors. / Nakayama, Keiko; Ishida, Noriko; Shirane, Michiko; Inomata, Akira; Inoue, Tomoaki; Shishido, Nobuyuki; Horii, Ikuo; Loh, Dennis Y.; Nakayama, Kei Ichi.

:: Cell, 巻 85, 番号 5, 31.05.1996, p. 707-720.

研究成果: ジャーナルへの寄稿記事

Nakayama, K, Ishida, N, Shirane, M, Inomata, A, Inoue, T, Shishido, N, Horii, I, Loh, DY & Nakayama, KI 1996, 'Mice Lacking p27Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors', Cell, 巻. 85, 番号 5, pp. 707-720. https://doi.org/10.1016/S0092-8674(00)81237-4
Nakayama, Keiko ; Ishida, Noriko ; Shirane, Michiko ; Inomata, Akira ; Inoue, Tomoaki ; Shishido, Nobuyuki ; Horii, Ikuo ; Loh, Dennis Y. ; Nakayama, Kei Ichi. / Mice Lacking p27Kip1 Display Increased Body Size, Multiple Organ Hyperplasia, Retinal Dysplasia, and Pituitary Tumors. :: Cell. 1996 ; 巻 85, 番号 5. pp. 707-720.
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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.",
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