Deletion of the p27Kip1 gene restores normal development in cyclin D1-deficient mice

Yan Geng, Qunyan Yu, Ewa Sicinska, Manjusri Das, Roderick T. Bronson, Piotr Sicinski

Research output: Contribution to journalArticlepeer-review

143 Scopus citations


D-type cyclins (cyclins D1, D2, and D3) are key components of cell cycle machinery in mammalian cells. These proteins are believed to drive cell cycle progression by associating with their kinase partners, cyclin-dependent kinases, and by directing phosphorylation of critical cellular substrates. In addition, D-cyclins play a kinase-independent role by sequestering cell cycle inhibitors p27Kip1 and p21Cip1. In the past, we and others generated cyclin D1-deficient mice and have shown that these mice display developmental abnormalities, hypoplastic retinas, and pregnancy-insensitive mammary glands. To test the significance of cyclin D1-p27Kip1 interaction within a living mouse, we crossed cyclin D1-deficient mice with mice lacking p27Kip1, and we generated double-mutant cyclin D1-/-p27-/- animals. Here we report that ablation of p27Kip1 restores essentially normal development in cyclin D1-deficient mice. Our results provide genetic evidence that p27Kip1 functions downstream of cyclin D1.

Original languageEnglish
Pages (from-to)194-199
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number1
StatePublished - 2 Jan 2001
Externally publishedYes


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