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Mol Genet Metab. 2016 Sep;119(1-2):37-43. doi: 10.1016/j.ymgme.2016.06.013. Epub 2016 Jun 30.

CBP/p300 acetyltransferase activity in hematologic malignancies.

Author information

1
Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.
2
Division of Hematology/Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: kmsakamo@stanford.edu.

Abstract

CREB binding protein (CBP) and p300 are critical regulators of hematopoiesis through both their transcriptional coactivator and acetyltransferase activities. Loss or mutation of CBP/p300 results in hematologic deficiencies in proliferation and differentiation as well as disruption of hematopoietic stem cell renewal and the microenvironment. Aberrant lysine acetylation mediated by CBP/p300 has recently been implicated in the genesis of multiple hematologic cancers. Understanding the effects of disrupting the acetyltransferase activity of CBP/p300 could pave the way for new therapeutic approaches to treat patients with these diseases.

KEYWORDS:

CBP; CREB-binding protein; Hematologic malignancies; Lysine acetyltransferase activity; Targeted therapy; p300

PMID:
27380996
DOI:
10.1016/j.ymgme.2016.06.013
[Indexed for MEDLINE]

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