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Forced expression of cyclin D1 does not compensate for Id2 deficiency in the mammary gland
Author(s) -
Mori Seiichi,
Inoshima Kenji,
Shima Yoko,
Schmidt Emmett V.,
Yokota Yoshifumi
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00906-2
Subject(s) - cyclin d1 , biology , cyclin b , mammary gland , cyclin d , cyclin , cancer research , ectopic expression , cyclin a , cell cycle , genetically modified mouse , cyclin a2 , microbiology and biotechnology , cyclin e1 , carcinogenesis , cyclin e , endocrinology , medicine , transgene , cancer , cell culture , breast cancer , genetics , gene
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.