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Publication : Transcription factor EBF restricts alternative lineage options and promotes B cell fate commitment independently of Pax5.

First Author  Pongubala JM Year  2008
Journal  Nat Immunol Volume  9
Issue  2 Pages  203-15
PubMed ID  18176567 Mgi Jnum  J:131602
Mgi Id  MGI:3774052 Doi  10.1038/ni1555
Citation  Pongubala JM, et al. (2008) Transcription factor EBF restricts alternative lineage options and promotes B cell fate commitment independently of Pax5. Nat Immunol 9(2):203-15
abstractText  Alternative lineage restriction and B cell fate commitment require the transcription factor Pax5, but the function of early B cell factor (EBF) in these processes remains mostly unexplored. Here we show that in the absence of EBF, 'expandable' and clonal lymphoid progenitor cells retained considerable myeloid potential. Conversely, ectopic expression of EBF in multipotential progenitor cells directed B cell generation at the expense of myeloid cell fates. EBF induced Pax5 and antagonized expression of genes encoding the transcription factors C/EBPalpha, PU.1 and Id2. Notably, sustained expression of EBF in Pax5-/- hematopoietic progenitor cells was sufficient to block their myeloid and T lineage potential in vivo. Furthermore, in Pax5-/- pro-B cells, higher EBF expression repressed alternative lineage genes. Thus, EBF can restrict alternative lineage 'choice' and promote commitment to the B cell fate independently of Pax5.
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