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Leuk Lymphoma. 2009 May;50(5):816-28. doi: 10.1080/10428190902836107.

The Spt-Ada-Gcn5-acetyltransferase complex interaction motif of E2a is essential for a subset of transcriptional and oncogenic properties of E2a-Pbx1.

Author information

Department of Medicine I and Pharmacology I, University Hospital Freiburg, Freiburg, Germany.

Erratum in

  • Leuk Lymphoma. 2009 Jul;50(7):1235. Duchniewicz, Marlena [removed].
  • Leuk Lymphoma. 2009 Nov;50(11):1904. Sykes, David P [corrected to Sykes, David B].


The oncogene E2a-Pbx1 is formed by the t(1;19) translocation, which joins the N-terminal transactivation domain of E2a with the C-terminal homeodomain of PBX1. The goal of this work was to elucidate the mechanisms by which E2a-Pbx1 can lead to deregulated target gene expression. For reporter constructs it was shown that E2a-Pbx1 can activate transcription through homodimer elements (TGATTGAT) or through heterodimer elements with Hox proteins (e.g. TGATTAAT). We show a novel mechanism by which E2a-Pbx1 activates transcription of EF-9 using a promoter in intron 1 of the EF-9 gene, resulting in an aminoterminal truncated transcript. Our results indicate that the LDFS motif of E2a is essential for the transactivation of EF-9, but dispensable for transactivation of fibroblast growth factor 15. The E2a LDFS motif was also essential for proliferation of NIH3T3 fibroblasts but was dispensable for the E2a-Pbx1-induced differentiation arrest of myeloid progenitors.

[Indexed for MEDLINE]

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