The gene CBP (CREB binding protein) is mapped to human chromosome 16p13.[1]
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CBP is a transcriptional coactivator. The protein is a link between the DNA-associated transcription factors and the RNA polymerase 2 complex. It also exhibits histone acetyltransferase activity.[2]
PF-CBP1 is potent and highly-selective inhibitor of the bromodomain of CREB binding protein (CBP BRD) that down regulates targets of CBP in macrophages primary neurons. Also, PF-CBP1 significantly reduces levels of RGS4 mRNA levels in neurons.
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11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
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Not applicable
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The bromodomain and extra terminal (BET) family of bromodomains have been the focus of extensive research, leading to the development of many potent, selective chemical probes and recent clinical assets. The profound biology associated with BET bromodomain inhibition has provided
Rubinstein-Taybi syndrome (RSTS) is a rare autosomal dominant congenital disorder (prevalence, 1:125000-720000) characterized by broad thumbs and halluces, facial dysmorphism, psychomotor development delay, skeletal defects, abnormalities in the posterior fossa, and short stature. The purpose of this study was to
Spontaneous complete and sustained remission of a rearrangement CBP (16p13)-positive disseminated congenital myelosarcoma.
Bromodomains are involved in transcriptional regulation through the recognition of acetyl lysine modifications on diverse proteins. Selective pharmacological modulators of bromodomains are lacking, although the largely hydrophobic nature of the pocket makes these modules attractive targets for small-molecule inhibitors. This
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