Mouse models CBP and p300 are critical for normal embryonic development, as mice completely lacking either CBP or p300 protein, die at an early embryonic stage. In addition, mice which lack one functional copy (allele) of both the CBP and p300 genes (i.e. are heterozygous for both CBP and p300) and thus haveContinue Reading
Mutations in CBP, and to a lesser extent p300, are the cause of Rubinstein-Taybi Syndrome, which is characterized by severe mental retardation. These mutations result in the loss of one copy of the gene in each cell, which reduces the amount of CBP or p300 protein by half. Some mutations lead toContinue Reading
Function in G protein signaling Some G proteins stimulate adenylate cyclase that results in elevation of cAMP. cAMP stimulates PKA, which consists of four subunits, two regulatory and two catalytic. Binding of cAMP to the regulatory subunits causes release of the catalytic subunits. These subunits can then enter the nucleus to interact with transcriptionalContinue Reading
Regulation of gene expression p300 and CBP are thought to increase gene expression in three ways: p300 regulates transcription by directly binding to transcription factors (see external reference for explanatory image). This interaction is managed by one or more of the p300 domains: the nuclear receptor interaction domain (RID), the CREB and MYB interaction domain (KIX), the cysteine/histidine regions (TAZ1/CH1Continue Reading
The p300-CBP coactivator family in humans is composed of two closely related transcriptional co-activating proteins (or coactivators): Both p300 and CBP interact with numerous transcription factors and act to increase the expression of their target genes. Protein structure p300 and CBP have similar structures. Both contain five protein interaction domains: the nuclear receptor interaction domain (RID), the KIX domain (CREB and MYB interactionContinue Reading
Histone acetyltransferase p300 also known as p300 HAT or E1A-associated protein p300 (where E1A = adenovirus early region 1A) also known as EP300 or p300 is an enzyme that, in humans, is encoded by the EP300 gene. It functions as histone acetyltransferase that regulates transcription of genes via chromatin remodeling by allowing histone proteins to wrap DNA less tightly. This enzyme plays an essential role in regulating cell growth and division, prompting cells toContinue Reading
Rubinstein-Taybi Syndrome (RTS) Type 1, which is caused by CBP mutations, for which over 500 different variations have been documented, accounts for approximately 55% of all cases, whereas RTS Type 2, which is caused by any of the nearly 120 different types of p300 mutations, accounts for only 8% of diagnosedContinue Reading
This gene is ubiquitously expressed and is involved in the transcriptional coactivation of many different transcription factors. CBP has two critical mechanisms by which it is able to regulate gene expression: as an acetyltransferase, and as a protein scaffold that helps recruit and construct the complexes that are necessary for transcription or chromatinContinue Reading
ActrNuclear receptor coactivator ACTR is a novel histone acetyltransferase and forms a multimeric activation complex with P/CAF and CBP/p300.Karamouzis MV, Konstantinopoulos PA, Papavassiliou AG (April 2007). “Roles of CREB-binding protein (CBP)/p300 in respiratory epithelium tumorigenesis”. Cell Research. 17 (4): 324–332. doi:10.1038/cr.2007.10. PMID 17372613. S2CID 36084602.Dyson HJ, Wright PE (March 2016). “Role of Intrinsic Protein Disorder in the Function and Interactions of theContinue Reading
Cyclic adenosine monophosphate Response Element Binding protein Binding Protein (CREB-binding protein), also known as CREBBP or CBP or KAT3A, is a coactivator encoded by the CREBBP gene in humans, located on chromosome 16p13.3. CBP has intrinsic acetyltransferase functions; it is able to add acetyl groups to both transcription factors as well as histone lysines, the latter of which has been shown to alter chromatin structure making genesContinue Reading
Alzheimer’s Disease (AD) is a progressive neurodegenerative disease whose pathology is diagnosed based on the presence of neuritic amyloid beta (Aβ) plaques and neurofibrillary tau (τ) tangles. Because the exact causes of the disease are not clearly understood, there are a number of different mechanisms by which CBP (CREB-binding protein) isContinue Reading
