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Article

MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma development.

Blood - 19 Mar 2015

Sheikh Bilal N, Lee Stanley C W, El-Saafin Farrah, Vanyai Hannah K, Hu Yifang, Pang Swee Heng Milon, Grabow Stephanie, Strasser Andreas, Nutt Stephen L, Alexander Warren S, Smyth Gordon K, Voss Anne K, Thomas Tim

Abstract excerpt

The histone acetyltransferase MOZ (MYST3, KAT6A) is the target of recurrent chromosomal translocations fusing the MOZ gene to CBP, p300, NCOA3, or TIF2 in particularly aggressive cases of acute myeloid leukemia. In this study, we report the role of wild-type MOZ in regulating B-cell progenitor proliferation and hematopoietic malignancy. In the Eμ-Myc model of aggressive pre-B/B-cell lymphoma, the loss of just one...

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Share to B-Lymphocytes
Share to Cellular Senescence

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Haploinsufficiency

Share to Histone Acetyltransferases

Share to Lymphoma

Share to Proto-Oncogene Proteins c-myc

Share to Sequence Analysis, RNA

Share to Stem Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 25605372
DOI: 10.1182/blood-2014-08-594655
PMCID: PMC4440887

Genes

MYC
MEIS1
NCOA3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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