| First Author | Karaya K | Year | 2005 |
| Journal | Nucleic Acids Res | Volume | 33 |
| Issue | 6 | Pages | 1924-34 |
| PubMed ID | 15809228 | Mgi Jnum | J:99449 |
| Mgi Id | MGI:3582153 | Doi | 10.1093/nar/gki339 |
| Citation | Karaya K, et al. (2005) Regulation of Id2 expression by CCAAT/enhancer binding protein beta. Nucleic Acids Res 33(6):1924-34 |
| abstractText | Mice deficient for Id2, a negative regulator of basic helix-loop-helix (bHLH) transcription factors, exhibit a defect in lactation due to impaired lobuloalveolar development during pregnancy, similar to the mice lacking the CCAAT enhancer binding protein (C/EBP) beta. Here, we show that Id2 is a direct target of C/EBPbeta. Translocation of C/EBPbeta into the nucleus, which was achieved by using a system utilizing the fusion protein between C/EBPbeta and the ligand-binding domain of the human estrogen receptor (C/EBPbeta-ERT), demonstrated the rapid induction of endogenous Id2 expression. In reporter assays, transactivation of the Id2 promoter by C/EBPbeta was observed and, among three potential C/EBPbeta binding sites found in the 2.3 kb Id2 promoter region, the most proximal element was responsible for the transactivation. Electrophoretic mobility shift assay (EMSA) identified this element as a core sequence to which C/EBPbeta binds. Chromatin immunoprecipitation (ChIP) furthermore confirmed the presence of C/EBPbeta in the Id2 promoter region. Northern blotting showed that Id2 expression in C/EBPbeta-deficient mammary glands was reduced at 10 days post coitus (d.p.c.), compared with that in wild-type mammary glands. Thus, our data demonstrate that Id2 is a direct target of C/EBPbeta and provide insight into molecular mechanisms underlying mammary gland development during pregnancy. |
