| First Author | Park SR | Year | 2003 |
| Journal | Eur J Immunol | Volume | 33 |
| Issue | 12 | Pages | 3386-92 |
| PubMed ID | 14635047 | Mgi Jnum | J:87165 |
| Mgi Id | MGI:2683814 | Doi | 10.1002/eji.200324061 |
| Citation | Park SR, et al. (2003) p300 cooperates with Smad3/4 and Runx3 in TGFbeta1-induced IgA isotype expression. Eur J Immunol 33(12):3386-92 |
| abstractText | We have shown previously that Smad3 and Smad4 mediate TGF-beta1-induced IgA expression. In the present study, we examined the involvement of Runx3 in this process. Overexpression of Runx3 in mice increased germ-line alpha (GLalpha) transcription, and transcription was further augmented when B lymphoma and LPS-activated murine spleen cells were co-transfected with Smad3/4. Overexpression of Runx3 and Smad3/4 increased IgA secretion by both cell types in response to TGF-beta1. p300, which has histone acetyltransferase activity, further augmented TGF-beta1-induced GLalpha transcription promoted by Smad3/4 and Runx3. These observations were confirmed by examining the influence of Smad3/4, Runx3 and p300 on the expression of endogenous GLalpha and post-switch alpha transcripts.E1A, an inhibitor of p300, blocked both GLalpha promoter activity and the enhancement of endogenous GLalpha transcription by Smad3/4 and Runx3. We conclude that p300 cooperates with Smad3/4 and Runx3 in stimulating TGF-beta1-induced GLalpha transcription and subsequent IgA isotype expression, while E1A inhibits these cooperative effects. |
