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anti-Human CBP Antibodies:
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Ectopic expression of EP300 (show EP300 Antibodies)-ZNF384 (show ZNF384 Antibodies) and CREBBP-ZNF384 (show ZNF384 Antibodies) fusion altered differentiation of mouse hematopoietic stem and progenitor cells and also potentiated oncogenic transformation in vitro.our results indicate that gene fusion is a common class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 (show EP300 Antibodies) and CREBBP may cause epigenetic deregulation with potential for therapeutic targeting.
The CREBBP acetyltransferase is a haploinsufficient tumor suppressor in B-cell lymphoma.
Understanding the effects of disrupting the acetyltransferase activity of CBP/p300 could pave the way for new therapeutic approaches to treat patients with these diseases
How cancer cells use p300/CBP in their favor varies depending on the cellular context and is evident by the growing list of loss- and gain-of-function genetic alterations in p300 (show EP300 Antibodies) and CBP in solid tumors and hematological malignancies.[review]
Mutations of CREBBP and SOCS1 (show SOCS1 Antibodies) are independent prognostic factors in diffuse large B cell lymphoma; CREBBP and EP300 (show EP300 Antibodies) mutations remained significant to predict worse OS, PFS, and EFS (show EFS Antibodies).
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.
Enhancer-priming by MLL3/MLL4 (show MLL4 Antibodies) followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
the aPKC-CBP pathway is a homeostatic compensatory mechanism that modulates hippocampal neurogenesis and memory in an age-dependent manner in response to reduced CREB (show CREB1 Antibodies) activity.
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.
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.
This gene is ubiquitously expressed and is involved in the transcriptional coactivation of many different transcription factors. First isolated as a nuclear protein that binds to cAMP-response element binding protein (CREB), this gene is now known to play critical roles in embryonic development, growth control, and homeostasis by coupling chromatin remodeling to transcription factor recognition. The protein encoded by this gene has intrinsic histone acetyltransferase activity and also acts as a scaffold to stabilize additional protein interactions with the transcription complex. This protein acetylates both histone and non-histone proteins. This protein shares regions of very high sequence similarity with protein p300 in its bromodomain, cysteine-histidine-rich regions, and histone acetyltransferase domain. Mutations in this gene cause Rubinstein-Taybi syndrome (RTS). Chromosomal translocations involving this gene have been associated with acute myeloid leukemia. Alternative splicing results in multiple transcript variants encoding different isoforms.
, CREB binding protein (Rubinstein-Taybi syndrome)