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CBP/p300 acetyltransferase activity in hematologic malignancies

Journal

MOLECULAR GENETICS AND METABOLISM
Volume 119, Issue 1-2, Pages 37-43

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ymgme.2016.06.013

Keywords

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

Funding

  1. Alex's Lemonade Stand Foundation for Childhood Cancer Pediatric Oncology Student Training award
  2. Stanford University
  3. St. Baldrick's Foundation
  4. Bear Necessities Pediatric Cancer
  5. Ventura Foundation
  6. NIH [R01 HL75826]
  7. Maxfield Foundation
  8. SPARK program
  9. Child Health Research Institute Lucile Packard Foundation for Children's Health
  10. Leukemia and Lymphoma Society of America [SLP-8009-15]
  11. Pediatric Cancer Research Foundation
  12. Hyundai Hope On Wheels [02500CA]
  13. USC Parker Hughes Institute for Childhood Cancer Research/William Lawrence & Blanche Hughes Foundation

Ask authors/readers for more resources

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. (C) 2016 Elsevier Inc. All rights reserved.

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