© 2005 BMJ Publishing Group Ltd
LETTER TO JMG
CBP truncating mutations in ovarian cancer
1 Departments of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN, USA
2 Departments of Pediatrics, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN, USA
3 Departments of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN, USA
Correspondence to:
Correspondence to:
Dr F J Couch
Mayo Clinic, Department of Laboratory Medicine and Pathology, 200 First Street SW, Rochester, MN 55905, USA; couch.fergus@mayo.edu
Revised version received 7 September 2004
Accepted 8 September 2004
Keywords: CBP; dHPLC; mutations; ovarian cancer
| The first 150 words of the full text of this article appear below. |
The CBP gene (OMIM #600140) encodes the 2441 amino acid cyclic AMP response element binding protein (CREB) binding protein (Mr 265 000) that functions as an essential co-activator for a number of transcription factors.1 In particular, CBP, like its homologue EP300, enhances gene transcription by linking sequence specific transcription factors to transcription factor IIB and the RNA polymerase II holoenzyme.2 CBP can also promote gene transcription by acetylation of histones through its histone acetyltransferase activity (HAT)3 and by acetylation of specific transcription factors such as p53.4–6 Several lines of evidence suggest the involvement of CBP in tumour formation. CBP interacts with the human T cell leukaemia virus (HTLV) Tax protein and v-myb to induce viral and cellular genes that promote cell transformation, while adenovirus E1A, simian virus SV40 Tag, and human papillomavirus (HPV) E6 bind to CBP and inhibit its co-activator function. CBP is also known to modulate the actions
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