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Blood, 15 September 2005, Vol. 106, No. 6, pp. 1995-2001.
Prepublished online as a Blood First Edition Paper on May 26, 2005; DOI 10.1182/blood-2004-12-4744.
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Submitted December 14, 2004
Accepted May 11, 2005
Inhibition of EBF function by active Notch signaling reveals a novel regulatory pathway in early B-cell development
Emma M Smith, Peter Akerblad, Tom Kadesch, Hakan Axelson, and Mikael Sigvardsson*
Department for Stem Cell Biology, Lund University, Lund, Sweden
Department of Molecular Pharmacology, AstraZeneca R&D Molndal, Molndal, Sweden
Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Department of Laboratory Medicine, Division of Molecular Medicine, Lund University, University Hospital, Malmo, Sweden
* Corresponding author; email: mikael.sigvardsson{at}stemcell.lu.se.
The Notch signaling pathway is involved in several lineage commitment and differentiation events. One of these is fate determination of the common lymphoid progenitor, promoting T cell development at the expense of B cell differentiation. This process has been suggested to rely on Notch to inhibit E-proteins, which are crucial for early B cell development. Here we report that Notch signaling also modulates the function of the transcription factor EBF. Transient transfection of intracellular Notch1 (Notch1-IC) into a pre-B cell line resulted in the down regulation of EBF regulated promoters, and diminished the capacity of EBF to activate these promoters in an epithelial cell line. This correlated with a reduction in EBF's ability to bind DNA. Ligand-induced stimulation of endogenous Notch receptors with Delta-4, mimicked the activity of Notch1-IC towards EBF. These data suggest that Notch signaling may affect B- versus T-lineage commitment by the targeting of both EBF and E2A.
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