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C646 treatment attenuated ETV1 protein expression and inactivated KIT-dependent pathways. Taken together, the present study suggests that CBP/p300 may serve as novel antineoplastic targets and that use of the selective HAT inhibitor C646 is a promising antitumor strategy for Gastrointestinal stromal tumors.
The CREBBP gene is believed to be the dosage-sensitive critical gene responsible for the reciprocal duplication and deletion syndrome
Results show that CREBBP was the most frequent target of epigenetic modification in juvenile myelomonocytic leukemia.
Data show that mutation of key residues in the binding site abolishes binding and that small ubiquitin-like modifier 1 (SUMO1 (show SUMO1 Proteins)) can simultaneously and non-cooperatively bind both the ZZ domain and a canonical SIM (show SIM2 Proteins) motif of CREB-binding protein (CBP/p300).
Cyclic AMP Response Element Binding Protein Mediates Pathological Retinal Neovascularization via Modulating DLL4 (show DLL4 Proteins)-NOTCH1 (show NOTCH1 Proteins) Signaling
high expression of both CREB-binding protein and cleavage and polyadenylation specific factor 4 (show CPSF4 Proteins) predicted a poor prognosis in the patients with lung adenocarcinomas.
RFPL3 and CBP have roles in upregulating hTERT activity and promoting lung cancer growth
Disruption of beta-catenin (show CTNNB1 Proteins)/CBP signaling inhibits human airway epithelial-mesenchymal transition and repair.
Intrinsic protein disorder plays a prominent role in the function and interactions of the transcriptional co-activators CBP and p300 (show EP300 Proteins). (Review)
42 new CREBBP mutations were reported in 46 Rubinstein-Taybi syndrome patients.
Study demonstrates that CBP binds directly to RNAs in vivo and in vitro. RNAs bound to CBP in vivo include a large number of eRNAs. Using steady-state histone acetyltransferase (HAT) assays, study shows that an RNA binding region in the HAT domain of CBP-a regulatory motif unique to CBP/p300-allows RNA to stimulate CBP's HAT activity.
We focused on genomic loci bound by the neuronal activity-regulated coactivator CREBBP, and we measured enhancer and promoter activities both before and after neuronal activation
Data suggest that mechanisms involving CBP histone acetyltransferase-mediated lysine acetylation of nuclear proteins support selectively long-term encoding in the medial prefrontal cortex circuits
Ajuba (show AJUBA Proteins) recruits p300/CBP via its LIM (show PDLIM5 Proteins) domain and facilitates p300/CBP binding to PPARg (show PPARG Proteins). Moreover, Ajuba (show AJUBA Proteins), PPARg (show PPARG Proteins), p300/CBP can cooperatively occupy the PPARg (show PPARG Proteins) target promoters and concomitantly increases histone acetylation at these loci.
Recognition of the disordered TP53 (show TP53 Proteins) transactivation domain by the transcriptional adapter zinc finger domains of CREB-binding protein.
Results indicate that loss of CBP CH1 domain function contributes to Rubinstein-Taybi Syndrome (RTS (show RECQL4 Proteins)), and possibly Autism spectrum disorders (ASDs), and that this domain plays an essential role in normal motor function, cognition and social behavior.
Tlx3 (show TLX3 Proteins) promotes glutamatergic neuronal subtype specification through direct interactions with the chromatin modifier CBP.
This study demonstrated that cbp increase in skeletal muscle in muscle atrophy.
PAG is constitutively phosphorylated in resting T cells and rapidly dephosphorylated once the TCR is engaged.
This gene encodes for a light absorbing visual pigment of the opsin gene family. The encoded protein is called red cone photopigment or long-wavelength sensitive opsin. Opsins are G-protein coupled receptors with seven transmembrane domains, an N-terminal extracellular domain, and a C-terminal cytoplasmic domain. This gene and the medium-wavelength opsin gene are tandemly arrayed on the X chromosome and frequent unequal recombination and gene conversion may occur between these sequences. X chromosomes may have fusions of the medium- and long-wavelength opsin genes or may have more than one copy of these genes. Defects in this gene are the cause of partial, protanopic colorblindness.
CREB binding protein (Rubinstein-Taybi syndrome)
, CREB-binding protein
, cone dystrophy 5 (X-linked)
, long-wave-sensitive opsin 1
, red cone photoreceptor pigment
, red-sensitive opsin
, Csk-binding protein
, phosphoprotein associated with glycosphingolipid-enriched microdomains 1
, phosphoprotein transmembrane adaptor 1
, phosphoprotein-associated with GEMs
, transmembrane phosphoprotein Cbp