p300/CBP and cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-05-24

AUTHORS

Narayanan Gopalakrishna Iyer, Hilal Özdag, Carlos Caldas

ABSTRACT

p300 and cyclic AMP response element-binding protein (CBP) are adenoviral E1A-binding proteins involved in multiple cellular processes, and function as transcriptional co-factors and histone acetyltransferases. Germline mutation of CBP results in Rubinstein–Taybi syndrome, which is characterized by an increased predisposition to childhood malignancies. Furthermore, somatic mutations of p300 and CBP occur in a number of malignancies. Chromosome translocations target CBP and, less commonly, p300 in acute myeloid leukemia and treatment-related hematological disorders. p300 mutations in solid tumors result in truncated p300 protein products or amino-acid substitutions in critical protein domains, and these are often associated with inactivation of the second allele. A mouse model confirms that p300 and CBP function as suppressors of hematological tumor formation. The involvement of these proteins in critical tumorigenic pathways (including TGF-β, p53 and Rb) provides a mechanistic route as to how their inactivation could result in cancer. More... »

PAGES

4225-4231

References to SciGraph publications

  • 2000-01-21. c-Myb acetylation at the carboxyl-terminal conserved domain by transcriptional co-activator p300 in ONCOGENE
  • 2000-05-23. CBP/p300 histone acetyl-transferase activity is important for the G1/S transition in ONCOGENE
  • 1996-09. The translocation t(8;16)(p11;p13) of acute myeloid leukaemia fuses a putative acetyltransferase to the CREB–binding protein in NATURE GENETICS
  • 2000-01. Analysis of the P300/CBP-Associated Factor (PCAF) Gene in Astrocytic Tumors in JOURNAL OF NEURO-ONCOLOGY
  • 1999-10-08. Function for p300 and not CBP in the apoptotic response to DNA damage in ONCOGENE
  • 1997-06. Binding and modulation of p53 by p300/CBP coactivators in NATURE
  • 1994-11. Loss of heterozygosity on chromosome 22 in ovarian carcinoma is distal to and is not accompanied by mutations in NF2 at 22q12 in BRITISH JOURNAL OF CANCER
  • 1996-12. The CBP co-activator is a histone acetyltransferase in NATURE
  • 2001-01. The monocytic leukemia zinc finger protein MOZ is a histone acetyltransferase in ONCOGENE
  • 2000-07-21. Smad-dependent stimulation of type I collagen gene expression in human skin fibroblasts by TGF-β involves functional cooperation with p300/CBP transcriptional coactivators in ONCOGENE
  • 2001-01-23. Fusion of MOZ and p300 histone acetyltransferases in acute monocytic leukemia with a t(8;22)(p11;q13) chromosome translocation in LEUKEMIA
  • 1997-12-18. Detection of CBP rearrangements in acute myelogenous leukemia with t(8;16) in LEUKEMIA
  • 2002-10-29. Mutation analysis of CBP and PCAF reveals rare inactivating mutations in cancer cell lines but not in primary tumours in BRITISH JOURNAL OF CANCER
  • 2000-03. Mutations truncating the EP300 acetylase in human cancers in NATURE GENETICS
  • 1995-07. Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP in NATURE
  • 2000-01. The language of covalent histone modifications in NATURE
  • 1998-12. Regulation of activity of the transcription factor GATA-1 by acetylation in NATURE
  • 1996-07. A p300/CBP-associated factor that competes with the adenoviral oncoprotein E1A in NATURE
  • 2001-06-18. Acetylation control of the retinoblastoma tumour-suppressor protein in NATURE CELL BIOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1207118

    DOI

    http://dx.doi.org/10.1038/sj.onc.1207118

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1034792476

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15156177


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