Nuclear localization of v-Abl leads to complex formation with cyclic AMP response element (CRE)-binding protein and transactivation through CRE motifs

Maria C. Birchenall-Roberts, Francis W. Ruscetti, James J. Kasper, Daniel C. Bertolette, Young Do Yoo, Ok Sun Bang, M. Scot Roberts, Jennifer M. Turley, Douglas K. Ferris, Seong Jin Kim

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Deregulated expression of v-abl and BCR/abl genes has been associated with myeloproliferative syndromes and myelodysplasia, both of which can progress to acute leukemia. These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v-Abl protein with the transcriptional regulator cyclic AMP response element-binding protein (CREB). We have mapped the specific domains within each of the proteins responsible for this interaction. We have shown that complex formation is a prerequisite for transcriptional potentiation of CREB. Transient overexpression of the homologous cellular protein c-Abl also results in the activation of promoters containing an intact CRE. These observations identify a novel function for v- Abl, that of a transcriptional activator that physically interacts with a transcription factor.

Original languageEnglish
Pages (from-to)6088-6099
Number of pages12
JournalMolecular and cellular biology
Volume15
Issue number11
DOIs
Publication statusPublished - 1995 Nov

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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