1: J Virol. 1997 Dec;71(12):9778-81. Overexpression of A-myb induces basic fibroblast growth factor-dependent proliferation of chicken neuroretina cells. Turque N, Plaza S, Klempnauer KH, Saule S. CNRS EP560, Institut Pasteur de Lille, France. A-Myb behaves similarly to c-Myb in chicken neuroretina cells in its ability to induce fibroblast-like differentiation, to promote growth in the presence of basic fibroblast growth factor (bFGF), and to induce Pax-6 and mim-1 expression. The one difference between c-Myb and A-Myb in these cells is that the former but not the latter protein causes colony formation in soft agar in the presence of bFGF. PMID: 9371644 [PubMed - indexed for MEDLINE] --------------------------------------------------------------- 2: Oncogene. 1995 Jan 19;10(2):329-40. C-Myb acts as transcriptional activator of the quail PAX6 (PAX-QNR) promoter through two different mechanisms. Plaza S, Turque N, Dozier C, Bailly M, Saule S. Laboratoire de Differenciation Cellulaire et Moleculaire, CNRS EP56 Institut Pasteur, Lille, France. To understand the regulation of the Pax-6 gene, which plays an important role in eye development, we have characterized the promoter region of the quail Pax-6(Pax-QNR) gene. In addition to TATA and CAAT boxes, sequence analysis revealed several putative cis-regulatory elements among which three myb-responsive elements (MRE). C-myb encodes a nuclear, DNA-binding phosphoprotein that functions as transcriptional regulator. Co-transfection in quail embryo cells of the Pax-QNR/pax-6 promoter with a vector expressing the 75 kDa c-myb protein resulted in an increase in Pax-QNR promoter activity. By footprinting experiments we identified multiple binding sites for the myb protein within the promoter region. Protein containing the myb DNA-binding domain fused to the VP16-transactivation domain was fully efficient in Pax-QNR promoter transactivation, demonstrating that myb can transactivate through a direct binding on DNA. However, a myb truncated protein devoid of DNA-binding domain was also able to transactivate the Pax-QNR promoter. These results show that this promoter can be transactivated by the myb protein directly as well as indirectly. Finally we show by in situ hybridization that c-myb is strongly expressed in the developing neuroretina, simultaneously with Pax-QNR. These observations suggest that the c-myb protein may be a regulator of Pax-QNR/pax-6. PMID: 7838532 [PubMed - indexed for MEDLINE] ---------------------------------------------------------------