Regular ArticleConstruction of a 1.2-Mb Contig Surrounding, and Molecular Analysis of, the Human CREB-Binding Protein (CBP/CREBBP) Gene on Chromosome 16p13.3☆
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Cited by (62)
Protein lysine acetyltransferase CBP/p300: A promising target for small molecules in cancer treatment
2024, Biomedicine and PharmacotherapyOpposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma
2018, Developmental CellCitation Excerpt :We report here on opposing effects of CREBBP mutations during cerebellar development that underlie both the pathogenesis of RTS-associated cerebellar malformations and the development of adult SHH MB. Germline mutations of CREBBP are associated with the developmental disorder RTS (Giles et al., 1997; Petrij et al., 1995). Apart from the known predisposition for cancer development, increasing evidence suggests that cerebellar malformations such as hypoplasia and Dandy-Walker-like alterations are frequent findings in RTS (Greco et al., 2009; Bonioli et al., 1989).
CBP/p300 acetyltransferase activity in hematologic malignancies
2016, Molecular Genetics and MetabolismCitation Excerpt :CREB binding protein (CBP) is encoded by a 190 kb gene located on chromosome 16p13.3. Transcription yields a 7.3 kb mRNA, which is translated into a protein of 2442 amino acid residues in humans [1,2]. The major protein domains of CBP include: the nuclear receptor interaction domain, the CREB-interacting kinase-inducible domain interacting (KIX) domain, three cysteine/histidine (CH) rich domains, a cyclin-dependent kinase inhibitor-reactive domain (CRD1) involved in cell cycle regulation and transcriptional suppression, a bromodomain (BRD) shown to recognize acetylated lysines, a 380 residue protein lysine acetyltransferase (KAT) domain, and a nuclear receptor coactivator binding domain (NCBD), also known as interferon binding domain (IBiD) [3–15] (Fig. 1).
Disruption of the CREBBP gene and decreased expression of CREB, NFκB p65, c-JUN, c-FOS, BCL2 and c-MYC suggest immune dysregulation
2013, Human ImmunologyCitation Excerpt :Its nomenclature is based on the interaction of the CREB protein with nuclear CREBBP [12]. The CREBBP gene has 31 exons, occupies approximately 159 kb of genomic DNA and encodes a protein of 265 kDa with 2442 amino acids [18]. CREBBP gene mutations lead to inactivation of one allele in patients with Rubinstein Taybi syndrome (RTs) [40,41].
Germline mosaicism in Rubinstein-Taybi syndrome
2013, GeneCitation Excerpt :CREBBP and EP300 are transcriptional coactivators (Goodman and Smolik, 2000). Conserved domains of CREBBP contain the histone acetyltransferase (HAT) domain and the plant homeodomain type zinc finger (PHD-ZF) (Giles et al., 1997; Kalkhoven et al., 2003; Murata et al., 2001; Roelfsema and Peters, 2007). CREBBP deficiency, caused by a mutation of one of the two CREBBP alleles in most patients, is one of the genetic etiologies of RSTS.
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The work presented in this report supports and extends the research presented by Soodet al.,pp. 83–95 of this issue. These two manuscripts combined describe more than 2 contiguous Mb of chromosome 16p13.3.
- 2
The first two authors contributed equally to this work.
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To whom correspondence should be addressed at Department of Human Genetics, Sylvius Laboratories, Leiden University, Wassenaarseweg 72, 2333 AL Leiden, The Netherlands. Telephone: 31-71-5276203. Fax: 31-71-5276075. E-mail: [email protected]. leidenuniv.nl.