Open AccessNuclear Localization of v-Abl Leads to Complex Formation with Cyclic AMP Response Element (CRE)-Binding Protein and Transactivation through CRE Motifs
Author(s) -
Maria C. Birchenall-Roberts,
Francis W. Ruscetti,
J Kasper,
Daniel C. Bertolette,
Yound Do Yoo,
OkSun Bang,
Margo Roberts,
Jennifer M. Turley,
Douglas K. Ferris,
SeongJin Kim
Publication year - 1995
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.15.11.6088
Subject(s) - biology , transactivation , transcription factor , abl , activator (genetics) , microbiology and biotechnology , response element , creb , gene product , creb binding protein , promoter , gene expression , gene , signal transduction , genetics , tyrosine kinase
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.