Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human CBP Antibodies:
anti-Mouse (Murine) CBP Antibodies:
anti-Rat (Rattus) CBP Antibodies:
Go to our pre-filtered search.
We conclude that patients with missense mutations in this specific CREBBP region show a phenotype that differs substantially from that in patients with Rubinstein-Taybi syndrome, and may prove to constitute one (or more) separate entities.
Pre-eclampsia occurs in 12/52 mothers of EP300 (show EP300 Antibodies) mutated individuals versus in 2/59 mothers of CREBBP mutated individuals, making pregnancy with an EP300 (show EP300 Antibodies) mutated fetus the strongest known predictor for pre-eclampsia
Earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies.
Data show that specifically inhibiting the interaction between CBP and catenin with ICG-001 results in the differentiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs).
5-FU promotes global histone de-acetylation by enhancing the degradation of p300/CBP in colorectal neoplasms.
CREBBP mutations were associated with inferior progression-free survival (PFS), whereas mutations in previously unreported HVCN1 (show HVCN1 Antibodies), a voltage-gated proton channel-encoding gene and B-cell receptor signaling modulator, were associated with improved PFS.
the rate-limiting transition state for binding between the TAZ1 (show TAZ Antibodies) domain of CREB binding protein and the intrinsically disordered transactivation domain of STAT2 (show STAT2 Antibodies) (TAD (show CRTAM Antibodies)-STAT2 (show STAT2 Antibodies)) by site-directed mutagenesis and kinetic experiments (Phi-value analysis) and found that the native protein-protein binding interface is not formed at the transition state for binding.
In targeted sequencing, a disruptive mutation of TNFAIP3 (show TNFAIP3 Antibodies) was the most common alteration (54%), followed by mutations of TBL1XR1 (show TBL1XR1 Antibodies) (18%) and cAMP response element binding proteins (CREBBP) (17%).
A mosaic variant in CREBBP identified as pathogenic in a patient with overlapping clinical features of Rubinstein-Taybi and Filippi syndromes tested negative for CKAP2L.
CREBBP-BCORL1 (show BCORL1 Antibodies) fusion is associated with ossifying fibromyxoid tumors.
High CBP-P300 expression is associated with lymphoma.
This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 (show BCL2 Antibodies) overexpression to promote B-cell lymphoma.
Data (including data from studies of hydrogen-deuterium exchange coupled to mass spectrometry in presence of denaturants) suggest that, for peptide fragments of human ACTR (show NCOA3 Antibodies) and mouse Crebbp representing disordered interaction domains, exchange rates are changed dramatically by high concentrations of denaturants guanidinium chloride or urea. (ACTR (show NCOA3 Antibodies) = activator of thyroid and retinoid receptor; Crebbp = CREB binding protein)
Crebbp+/- common myeloid progenitors and granulocyte/macrophage progenitors could trigger skewed myelopoiesis, myelodysplasia and late-onset acute myeloid leukemia (show BCL11A Antibodies).
Brd3 (show BRD3 Antibodies) knockout significantly decreased the recruitment of acetylase CBP to IL6 (show IL6 Antibodies) gene promoter, and the acetylation level of histone3 within IL6 (show IL6 Antibodies) gene promoter was repressed.
Inhibition of hypothalamic Cbp results in profound obesity and impaired glucose homeostasis, increased food intake, and decreased body temperature. In addition, these changes are accompanied by molecular evidence in the hypothalamus for impaired leptin (show LEP Antibodies) and insulin (show INS Antibodies) signaling, a shift from glucose to lipid metabolism, and decreased Pomc (show POMC Antibodies) mRNA, with no effect on locomotion.
our findings illustrate that Cbp is an important regulator of Csk (show CSK Antibodies) recruitment to the SFK Lyn (show LYN Antibodies) in Eporesponsive erythroid cells.
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 (show HAT Antibodies)) assays, study shows that an RNA binding region in the HAT (show HAT Antibodies) domain of CBP-a regulatory motif unique to CBP/p300-allows RNA to stimulate CBP's HAT (show HAT Antibodies) 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
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