The translocation t(8;16)(p11;p13) of acute myeloid leukaemia fuses a putative acetyltransferase to the CREB-binding protein

Julian Borrow, Vincent P. Stanton, J. Michael Andresen, Reinhard Becher, Frederick G. Behm, Raju S K Chaganti, Curt I. Civin, Christine Disteche, Ian Dubé, Anna Marie Frischauf, Doug Horsman, Felix Mitelman, Stefano Volinia, Ann E. Watmore, David E. Housman

Research output: Contribution to journalArticlepeer-review

Abstract

The recurrent translocation t(8;16)(p11;p13) is a cytogenetic hallmark for the M4/M5 subtype of acute myeloid leukaemia. Here we identify the breakpoint-associated genes. Positional cloning on chromosome 16 implicates the CREB-binding protein (CBP), a transcriptional adaptor/coactivator protein. At the chromosome 8 breakpoint we identify a novel gene, MOZ, which encodes a 2,004-amino-acid protein characterized by two C4HC3 zinc fingers and a single C2HC zinc finger in conjunction with a putative acetyltransferase signature. In-frame MOZ-CBP fusion transcripts combine the MOZ finger motifs and putative acetyltransferase domain with a largely intact CBR. We suggest that MOZ may represent a chromatin-associated acetyltransferase, and raise the possibility that a dominant MOZ-CBP fusion protein could mediate leukaemogenesis via aberrant chromatin acetylation.

Original languageEnglish (US)
Pages (from-to)33-41
Number of pages9
JournalNature Genetics
Volume14
Issue number1
DOIs
StatePublished - Sep 1996

ASJC Scopus subject areas

  • Genetics(clinical)
  • Genetics

Fingerprint Dive into the research topics of 'The translocation t(8;16)(p11;p13) of acute myeloid leukaemia fuses a putative acetyltransferase to the CREB-binding protein'. Together they form a unique fingerprint.

Cite this