期刊论文详细信息
FEBS Letters
Forced expression of cyclin D1 does not compensate for Id2 deficiency in the mammary gland
Mori, Seiichi1  Inoshima, Kenji1  Schmidt, Emmett V.2  Shima, Yoko1  Yokota, Yoshifumi1 
[1] Department of Biochemistry, Fukui Medical University, 23-3 Shimoaizuki, Matsuoka, Fukui 910-1193, Japan;Massachusetts General Hospital Cancer Center and the Children's Service, Massachusetts General Hospital, Building 149, 13th Street, Charlestown, MA 02129, USA
关键词: Id2;    Cyclin D1;    Mammary gland;    AD;    transactivation domain;    BD;    DNA binding domain;    BrdU;    bromodeoxyuridine;    cdk;    cyclin-dependent kinase;    CK18;    cytokeratin 18;    d.p.c.;    days post coitus;    MMTV;    mouse mammary tumor virus;    pRb;    retinoblastoma protein;    RT-PCR;    reverse transcription-polymerase chain reaction;    Tg;    transgenic;   
DOI  :  10.1016/S0014-5793(03)00906-2
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

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.

【 授权许可】

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