CBP/p300 acetyltransferase activity in hematologic malignancies

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


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.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural

MeSH terms

  • Acetylation
  • CREB-Binding Protein / genetics*
  • E1A-Associated p300 Protein / genetics*
  • Hematologic Neoplasms / genetics*
  • Hematologic Neoplasms / pathology
  • Hematopoiesis / genetics
  • Humans
  • Lysine / metabolism
  • Mutation
  • Transcription, Genetic*


  • CREB-Binding Protein
  • CREBBP protein, human
  • E1A-Associated p300 Protein
  • EP300 protein, human
  • Lysine