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Study demonstrated that the long intrinsically disordered regions (IDRs) linking the KIX domain and bromodomain of CBP (termed ID3) can potentially bind to several proteins and identified ZFP106 as a novel substrate for CBP-mediated acetylation. Further data showed that the fully disordered isolated ID3 transiently interacts with an IDR of ZFP106 in a fashion that both IDR regions are maintained.
Co-immunoprecipitation analysis and siRNA-mediated suppression of CREB expression indicated that phospho-CREB has a positive effect on pro-inflammatory gene expression in the crosstalk between BAFF- and TLR4-mediated signaling by forming trimeric complexes containing NF-kappaB, CBP, and CREB
CREBBP and p300 may contribute to genome stability by fine-tuning the functions of DNA damage signaling and DNA repair factors, thereby expanding their role as tumor suppressors. (Review)
This review is focused on the different targets and functions of p300/CBP in physiological and pathological processes, including lipogenesis, lipid export, gluconeogenesis, and liver fibrosis, also provided some nutrients as the regulator of p300/CBP for nutritional therapeutic approaches to treat liver diseases.
provide evidence that both CREBBP and EP300 are bona fide tumor suppressors that control MHCII expression and promote tumor immune control; mutational inactivation of CREBBP, but not of EP300, has additional cell-intrinsic engraftment and growth-promoting effects
BRD, PHD, and ZZ domains interact with SUMO-1 and Ubc9, and function as an intramolecular E3 ligase for SUMOylation of the cell cycle regulatory domain 1; the BRD is essential for histone H3 acetylation
CREBBP Mutation is associated with Rubinstein-Taybi Syndrome and Medulloblastoma.
The recruitment of COASY inhibits CBP-mediated TPX2 acetylation, promoting TPX2 degradation for mitotic exit.
GATA3 interacts with and is acetylated by the acetyltransferase CBP. The major acetylated site of GATA3 in lung adenocarcinoma cells is lysine 119.
The mechanism of CBP-CREB association via their pKID/KIX domains studied by molecular dynamics free energy simulations has been reported.
Our study demonstrated the association of low CREBBP expression with adverse clinical and biological features, poor prednisone response, high MRD levels and inferior outcomes in paediatric Chinese patients with ALL who were treated with the BCH- 2003 and CCLG- 2008 pro- tocols.
Knockdown of CREB suppressed the expression of matrix metallopeptidase (MMP)2/9.
mutation unlikely to be an early event in squamous cell carcinogenesis
Ectopic expression of EP300-ZNF384 and CREBBP-ZNF384 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 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 and CBP in solid tumors and hematological malignancies.[review]
Mutations of CREBBP and SOCS1 are independent prognostic factors in diffuse large B cell lymphoma; CREBBP and EP300 mutations remained significant to predict worse OS, PFS, and EFS.
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 mutated individuals versus in 2/59 mothers of CREBBP mutated individuals, making pregnancy with an EP300 mutated fetus the strongest known predictor for pre-eclampsia
Data suggest a role for CBP/p300 in testis determination mediated by control of histone acetylation at the Sry locus and reveal a novel element in the epigenetic control of Sry and mammalian sex determination.
this study elucidates the role of the aPKC-CBP pathway in modulating neurovascular remodeling and functional recovery following focal ischemic stroke.
Data (including data from studies in knockout and transgenic mice) suggest that Ep300 and Crebbp are limiting cofactors for pancreatic islet development (including gene expression regulation and cell proliferation), and hence for postnatal glucose homeostasis, with some functional redundancy. (Ep300 = E1A binding protein p300; Crebbp = CREB binding protein)
Enhancer-priming by MLL3/MLL4 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 activity.
Earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies.
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 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 and mouse Crebbp representing disordered interaction domains, exchange rates are changed dramatically by high concentrations of denaturants guanidinium chloride or urea. (ACTR = 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.
Brd3 knockout significantly decreased the recruitment of acetylase CBP to IL6 gene promoter, and the acetylation level of histone3 within IL6 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 and insulin signaling, a shift from glucose to lipid metabolism, and decreased Pomc 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) 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
Social isolation resulted in up-regulation of cbep expression in the cerebral cortex.
Cyclic AMP Response Element Binding Protein Mediates Pathological Retinal Neovascularization via Modulating DLL4-NOTCH1 Signaling
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 recruits p300/CBP via its LIM domain and facilitates p300/CBP binding to PPARg. Moreover, Ajuba, PPARg, p300/CBP can cooperatively occupy the PPARg target promoters and concomitantly increases histone acetylation at these loci.
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)