|Other Names||CREB-binding protein, CREBBP, CBP|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1077a was selected from the N-term region of human CREBBP. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Acetylates histones, giving a specific tag for transcriptional activation. Also acetylates non-histone proteins, like NCOA3 and FOXO1. Binds specifically to phosphorylated CREB and enhances its transcriptional activity toward cAMP-responsive genes. Acts as a coactivator of ALX1 in the presence of EP300. Acts as a circadian transcriptional coactivator which enhances the activity of the circadian transcriptional activators: NPAS2- ARNTL/BMAL1 and CLOCK-ARNTL/BMAL1 heterodimers. Acetylates PCNA; acetylation promotes removal of chromatin-bound PCNA and its degradation during nucleotide excision repair (NER) (PubMed:24939902).|
|Cellular Location||Cytoplasm. Nucleus. Note=Recruited to nuclear bodies by SS18L1/CREST. In the presence of ALX1 relocalizes from the cytoplasm to the nucleus|
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Provided below are standard protocols that you may find useful for product applications.
CREBBP is an acetyltransferase enzyme that acetylates histones, giving a specific tag for transcriptional activation. It also acetylates non-histone proteins, like NCOA3 coactivator. This protein mediates cAMP-gene regulation by binding specifically to phosphorylated CREB protein. CBP, as coactivator, augments the activity of phosphorylated CREB to activate transcription of cAMP-responsive genes. Chromosomal aberrations involving CREBBP may be a cause of acute myeloid leukemias. For example, MYST3-CREBBP may induce leukemia by inhibiting RUNX1-mediated transcription. Defects in CREBBP are also the cause of Rubinstein-Taybi syndrome (RSTS). RSTS is an autosomal dominant disorder characterized by craniofacial abnormalities, broad thumbs, broad big toes, mental retardation and a propensity for development of malignancies.
Cui, Q., et al., Oncogene 24(24):3864-3874 (2005).Gray, M.J., et al., Oncogene 24(19):3110-3120 (2005).Mayr, B.M., et al., J. Biol. Chem. 280(15):15103-15110 (2005).Roelfsema, J.H., et al., Am. J. Hum. Genet. 76(4):572-580 (2005).Furumatsu, T., et al., J. Biol. Chem. 280(9):8343-8350 (2005).
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