| First Author | Mori S | Year | 2003 |
| Journal | FEBS Lett | Volume | 551 |
| Issue | 1-3 | Pages | 123-7 |
| PubMed ID | 12965216 | Mgi Jnum | J:85412 |
| Mgi Id | MGI:2675143 | Doi | 10.1016/s0014-5793(03)00906-2 |
| Citation | Mori S, et al. (2003) Forced expression of cyclin D1 does not compensate for Id2 deficiency in the mammary gland. FEBS Lett 551(1-3):123-7 |
| abstractText | 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. |
