a protein acetyltransferase that can transcriptionally activate histones. Acetylates the NCOA3 coactivator. Binds specifically to phosphorylated CREB1 and enhances its transcriptional activity toward cAMP-responsive genes. Methylation of the KIX domain by CARM1 blocks association with CREB, blocking CREB signaling, and activating the apoptotic response. Found in a complex containing NCOA2, NCOA3, IKKA, IKKB, and IKBKG. Probably part of a complex with HIF1A and EP300. Interacts with the C-terminal region of CITED4. The TAZ-type 1 domain interacts with HIF1A. Interacts with MAF, SRCAP, CARM1, ELF3, MLLT7/FOXO4, N4BP2, NCOA1, NCOA3, NCOA6, PCAF, PELP1, PML, SMAD1, SMAD2, SMAD3, SPIB and TRERF1. Interacts with HTLV-1 Tax, p30II, and HIV-1 Tat. Interacts with KLF1; the interaction results in acetylation of KLF1 and enhancement of its transcriptional activity. Interacts with ZCCHC12. Interacts with DAXX; the interaction is dependent on CBP sumoylation and results in suppression of the transcriptional activiy via recruitment of HDAC2 to DAAX. Interacts with MTDH. Interacts with NFATC4. Interacts with MAFG; the interaction acetylates MAFG in the basic region and stimulates NFE2 transcriptional activity through increasing its DNA-binding activity. Interacts with IRF2; the interaction acetylates IRF2 and regulates its activity on the H4 promoter. Interacts via its N-terminus with the C-terminus of SS18L1. Interacts with MECOM. Chromosomal aberrations involving CBP may be a cause of acute myeloid leukemias. Known translocation partners include MYST3, MLL, and MYST4. MYST3-CBP fusion proteins may induce leukemia by inhibiting RUNX1-mediated transcription. Defects in CBP are a cause of Rubinstein-Taybi syndrome type 1 (RSTS1), an autosomal dominant disorder characterized by craniofacial abnormalities, broad thumbs, broad big toes, mental retardation and a propensity for development of malignancies. Note: This description may include information from UniProtKB.
Biological Process: embryonic digit morphogenesis; histone acetylation; N-terminal peptidyl-lysine acetylation; negative regulation of transcription from RNA polymerase II promoter; Notch signaling pathway; positive regulation of interferon type I production; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; protein amino acid acetylation; protein complex assembly; protein destabilization; regulation of apoptosis; regulation of lipid metabolic process; regulation of smoothened signaling pathway; regulation of transcription, DNA-dependent; response to hypoxia; stimulatory C-type lectin receptor signaling pathway; transcription initiation from RNA polymerase II promoter