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anti-Human CBP Antikörper:
anti-Mouse (Murine) CBP Antikörper:
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Human Polyclonal CBP Primary Antibody für ICC, IF - ABIN151846
Wu, Zhang, Cenciarini, Proietti, Amasino, Hong, Yang, Liao, Chiang, Kaklamani, Jeselsohn, Vadlamudi, Huang, Li, De Angelis, Fu, Elizalde, Schiff, Brown, Xu: Tamoxifen Resistance in Breast Cancer Is Regulated by the EZH2-ERα-GREB1 Transcriptional Axis. in Cancer research 2017
Human Polyclonal CBP Primary Antibody für ChIP, IP - ABIN151845
Li, Xu, Fu, Lei, Yao, Yang, Zhang, Washburn, Florens, Jaiswal, Wu, Mohan: DYRK1A interacts with histone acetyl transferase p300 and CBP and localizes to enhancers. in Nucleic acids research 2018
Data highlight an unforeseen link between CBP/P300 activity and the emergence of dystrophic phenotypes. They thereby identify CBP and P300 as mediators of adult muscle integrity and suggest a new lead for intervention in muscular dystrophy.
Enhancer activity requires CBP/P300 bromodomain-dependent histone H3K27 acetylation.
Data indicate that activation of beta-catenin-dependent signaling in chronic lung disease leads to changes in mucus and ciliated cell frequency and that P300 and CBP tune the beta-catenin signal to favor mucus cell differentiation.
CBP is a major modulator of dasatinib sensitivity; its targeting by small-molecule inhibitors shows promising preclinical efficacy increasing sensitivity to dasatinib in acute lymphoblastic leukemia
study to find frameshift mutations in repeats of CREBBP which had not been reported in gastric cancer (GC) and colorectal cancer (CRC) with microsatellite instability; also, analyzed expression of CREBBP in GC and CRC; findings suggest alteration of CREBBP gene by somatic mutation in the nucleotide repeat and expressional loss is not common in GC and CRC, and may not contribute to their development
The variant of the CREBBP gene is known to be causative of RSTS Type 1. The variant in the EP300 gene is benign since the father carried the same variant and exhibited no abnormalities. However, functional studies are required to investigate if this benign EP300 variant influences the phenotype in the presence of disease-causing CREBBP gene mutations.
CREBBP gene mutations are frequently detected in in situ follicular neoplasia.
Wild-type TRPM2 but not Ca(2+)-impermeable mutant E960D reconstituted phosphorylation and expression of Pyk2 and CREB in TRPM2-depleted cells exposed to doxorubicin. Results demonstrate that TRPM2 expression protects the viability of neuroblastoma through Src, Pyk2, CREB, and MCU activation, which play key roles in maintaining mitochondrial function and cellular bioenergetics
Data suggest that dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) functions in enhancer regulation by interacting with histone acetyltransferase p300 (p300)/CREB binding protein CREB (CBP) and modulating their activity.
By regulating CBP, Hsp27 maintained cell homeostasis and inhibited excessive inflammatory response.
Next generation sequencing identified two novel mutations in NIPBL and a frame shift mutation in CREBBP in three Chinese childre
We conclude that there is now more firm evidence that variants in these specific regions of CREBBP and EP300 result in a phenotype that differs from RSTS, and that this phenotype may be heterogeneous.
CBP may not play major role in the pathophysiology of Alzheimer's disease in Han Chinese.
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.
Crebbp Loss Accelerates Development of Small Cell Lung Cancer.
CBP is essential for interneuron development and the proper functioning of inhibitory circuitry in vivo.
PLY leads to the high expression of CERB-binding protein (CBP) which can lead to releasing of tumor necrosis factor alpha then enhance apoptosis of cells which is a significant factor leading to permeabilization of blood-brain barrier.
These results indicate how signaling pathways are altered to promote CD8(+) memory cell formation and rapid responses to and protection from repeat infections
In APP/PS1 transgenic mice, a model of Alzheimer disease, we analyzed CBP on its transcriptional activity and protein levels, finding a significant downregulation of both of them at 3-month-old mice. In addition, the downregulation of this molecule was associated with a decrease on acetylation levels of histone H3 in the hippocampus.
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.
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)