The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
IHC-P: Ready-to-use, treat for 30 min at RT.
Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Acetylates histones, giving a specific tag for transcriptional activation. Also acetylates non-histone proteins, like NCOA3 coactivator. 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.
Involvement in disease
Note=Chromosomal aberrations involving CREBBP may be a cause of acute myeloid leukemias. Translocation t(8;16)(p11;p13) with MYST3/MOZ; translocation t(11;16)(q23;p13.3) with MLL/HRX; translocation t(10;16)(q22;p13) with MYST4/MORF. MYST3-CREBBP may induce leukemia by inhibiting RUNX1-mediated transcription. Defects in CREBBP are a cause of Rubinstein-Taybi syndrome type 1 (RSTS1) [MIM:180849]. RSTS1 is an autosomal dominant disorder characterized by craniofacial abnormalities, broad thumbs, broad big toes, mental retardation and a propensity for development of malignancies.
Methylation of the KIX domain by CARM1 blocks association with CREB. This results in the blockade of CREB signaling, and in activation of apoptotic response. Phosphorylated upon DNA damage, probably by ATM or ATR. Sumoylation negatively regulates transcriptional activity via the recruitment of DAAX.
Cytoplasm. Nucleus. Recruited to nuclear bodies by SS18L1/CREST. In the presence of ALX1 relocalizes from the cytoplasm to the nucleus.