Journal
CELLULAR SIGNALLING
Volume 20, Issue 6, Pages 1151-1158Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2008.02.002
Keywords
ceap-16; BRD7; cellular proliferation; transcriptional regulation
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The centrosome associated protein Ceap-16 (also termed BLOS2) can accelerate the proliferation of mouse fibroblast NIH3T3 cells, which mechanism remains unclear. Here we identified tumor suppressor candidate BRD7 (bromodomain containing protein 7), which could negatively regulate cell proliferation and growth, as a novel Ceap-16-interacting protein. Ceap-16 and BRD7 interacted with each other both in vitro and in vivo. The C-terminus of BRD7 and the central region of Ceap-16 mediated the interaction. Through this binding, Ceap-16 could translocate from cytoplasm to the nucleus where it selectively inhibited the transcriptional suppression activity of BRD7 towards certain target genes including E2F3 and cyclin A. Moreover, Ceap-16, BRD7 and historic H3/H4 could form a complex and Ceap-16 did not compete with BRD7 binding to histories. These findings suggest a novel function for Ceap-16 in the transcriptional regulation through associating with BRD7. (C) 2008 Elsevier Inc. All rights reserved.
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