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FEBS Lett. 2003 Sep 11;551(1-3):123-7.

Forced expression of cyclin D1 does not compensate for Id2 deficiency in the mammary gland.

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Department of Biochemistry, Fukui Medical University, 23-3 Shimoaizuki, Matsuoka, 910-1193 Fukui, Japan.


Id2 and cyclin D1 share several biological activities, including inhibition of differentiation, stimulation of the G1-S transition in the cell cycle and stimulation of tumorigenesis. Mammary glands of Id2(-/-) mice display severely impaired lobulo-alveolar development during pregnancy, similarly to those of cyclin D1 null females. We investigated the functional relationship between Id2 and cyclin D1 in the mammary gland. Id2(-/-) mammary glands expressed a normal level of cyclin D1. No direct interaction of Id2 with cyclin D1 or its binding partner cdk4 was detected in mammalian two-hybrid assays. Ectopic expression of a cyclin D1 transgene did not rescue the mammary phenotype of Id2(-/-) mice. These results suggest that Id2 acts downstream or independently of cyclin D1 in the control of mammary cell proliferation during pregnancy.

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