p300/CBP and cancer

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Iyer N., ÖZDAĞ SEVGİLİ H., Caldas C.

ONCOGENE, cilt.23, sa.24, ss.4225-4231, 2004 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 23 Sayı: 24
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1038/sj.onc.1207118
  • Dergi Adı: ONCOGENE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.4225-4231
  • Anahtar Kelimeler: p300, CBP, mutations, translocations, RUBINSTEIN-TAYBI-SYNDROME, ACUTE MYELOID-LEUKEMIA, CREB-BINDING-PROTEIN, TUMOR-SUPPRESSOR GENE, TRANSCRIPTIONAL COACTIVATOR P300, ACUTE MONOCYTIC LEUKEMIA, CBP-INDUCED STIMULATION, HISTONE ACETYLTRANSFERASE, DNA-DAMAGE, CHROMOSOME-TRANSLOCATION
  • Ankara Üniversitesi Adresli: Hayır

Özet

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, soma tic 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-beta, p53 and Rb) provides a mechanistic route as to how their inactivation could result in cancer.