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anti-Human p300 Anticorps:
anti-Mouse (Murine) p300 Anticorps:
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Human Monoclonal p300 Primary Antibody pour ChIP, EM - ABIN152047
Eckner, Ludlow, Lill, Oldread, Arany, Modjtahedi, DeCaprio, Livingston, Morgan: Association of p300 and CBP with simian virus 40 large T antigen. dans Molecular and cellular biology 1996
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Human Monoclonal p300 Primary Antibody pour FACS, ICC - ABIN151948
Eckner, Yao, Oldread, Livingston: Interaction and functional collaboration of p300/CBP and bHLH proteins in muscle and B-cell differentiation. dans Genes & development 1996
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Human Polyclonal p300 Primary Antibody pour ChIP, ICC - ABIN152981
Julien, Carriere, Moreau, Roux: mTORC1-activated S6K1 phosphorylates Rictor on threonine 1135 and regulates mTORC2 signaling. dans Molecular and cellular biology 2010
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Human Monoclonal p300 Primary Antibody pour ChIP, ICC - ABIN152048
Eckner, Ewen, Newsome, Gerdes, DeCaprio, Lawrence, Livingston: Molecular cloning and functional analysis of the adenovirus E1A-associated 300-kD protein (p300) reveals a protein with properties of a transcriptional adaptor. dans Genes & development 1994
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Human Monoclonal p300 Primary Antibody pour ChIP-seq, ChIP - ABIN2668569
Dallas, Yaciuk, Moran: Characterization of monoclonal antibodies raised against p300: both p300 and CBP are present in intracellular TBP complexes. dans Journal of virology 1997
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Human Polyclonal p300 Primary Antibody pour DB, IHC (p) - ABIN537611
Jin, Jeon, Li, Lee, Choi, Kim, Lee, Bae: Transforming growth factor-beta stimulates p300-dependent RUNX3 acetylation, which inhibits ubiquitination-mediated degradation. dans The Journal of biological chemistry 2004
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Human Polyclonal p300 Primary Antibody pour IHC - ABIN6712156
Wu, Li, Li, Ti, Zhao, Si, Mei, Zhao, Fu, Han: LRP16 integrates into NF-κB transcriptional complex and is required for its functional activation. dans PLoS ONE 2011
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Human Polyclonal p300 Primary Antibody pour IHC - ABIN6712098
Zhang, Shen, Liu, Wang, Zhao, Zhang: Hypoxia-inducible factor 1-mediated human GATA1 induction promotes erythroid differentiation under hypoxic conditions. dans Journal of cellular and molecular medicine 2012
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Human Monoclonal p300 Primary Antibody pour ELISA, WB - ABIN966068
Stauffer, Chang, Huang, Dunn, Thayer: p300/CREB-binding protein interacts with ATR and is required for the DNA replication checkpoint. dans The Journal of biological chemistry 2007
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Human Monoclonal p300 Primary Antibody pour ELISA, WB - ABIN969098
Geiger, Sharma, Kim, Nyborg: The human T-cell leukemia virus type 1 tax protein confers CBP/p300 recruitment and transcriptional activation properties to phosphorylated CREB. dans Molecular and cellular biology 2008
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SP1 and P300 play an important role during decidualization.
The results represent a conserved mechanism, by which CtBP2 serves as a NADH-dependent repressor of the p300-Runx2 transcriptional complex and thus affects bone formation.
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.
P300 may play a key role in ARDS by positively regulating RORgammat transcription.
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.
p300 induces a dynamic hyper-acetylated chromatin state and promotes the formation of active enhancer elements in the non-coding genome, leading to a senescence-specific gene expression program.
Study shows that reduced levels of miRNA lethal 7d in idiopathic pulmonary fibrosis (IPF) compromise epigenetic gene silencing mediated by the ribonucleoprotein complex MiCEE. Hyperactive EP300 reduces nuclear HDAC1 and interferes with MiCEE function in IPF.
A better overview of the incidence of EP300-ZNF384 patients that shows that they have a distinct gene signature with concurrent up-regulation of JAK-STAT pathway, reduced expression of B-cell regulators and reduced DNA repair capacity.
he molecular dynamics (MD) simulation also performed, it reveals the conformational stability and the intermolecular interactions of C646 molecule in the active site of p300.
Data show the critical pathways regulating the expression of ADAMDEC1 and the roles of enhancer RNAs and mechanistically links E1A binding protein p300 (p300) and enhancer RNAs, which is dependent on NF-kappa B (NFkappaB).
Studies demonstrate that miR-500a-5p functions as a tumour suppressor in CRC by targeting the p300/YY1/HDAC2 axis, which contributes to the development of and provides new potential candidates for CRC therapy.
data explain how cellular signalling and the activation and dimerization of transcription factors control the activation of p300, and therefore explain why gene transcription is associated with chromatin acetylation
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.
findings demonstrate that RACK1 is involved in p300/GATA4-dependent hypertrophic responses in cardiomyocytes and is a promising therapeutic target for heart failure
As a crucial tumor promoter, p300 promotes cell proliferation, migration, and invasion in non-small cell lung cancer cells
Next-generation sequencing revealed specific mutations in EP300 to be associated with the mutational patterns in typical breast cancer genes and long-term outcome of triple-negative breast cancer patients.
While the primary tumours showed mutations in genes associated with cell adhesion and motility, brain metastases acquired mutations in adaptive, cytoprotective genes involved in response to cellular stress such as Keap-1, Nrf2 and P300, which are key players of the Keap1-Nrf2-ARE survival pathway.
Systems approach revealed that histone deacetylation is strongly associated with the suppression of EP300 target genes implicated in diabetes.
novel EP300 mutations were found in Rubinstein-Taybi 2 syndrome
p300 autoacetylation is associated with tongue neoplasms.
The data indicate that brachyury mediates acetylated H3K27 recruitment through a physical interaction with p300 during the mouse mesoderm development.
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.
Study in mouse model found that liver stiffness activates hepatic stellate cells differentiation into myofibroblasts, which required nuclear accumulation of p300.
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)
Here the authors report a lipopolysaccharide-induced NFkappaB enhanceosome in which TonEBP is required for the recruitment of p300. Increased expression of TonEBP enhances the NFkappaB activity and reduced TonEBP expression lowers it.
Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
Data show that LPS induces endoplasmic reticulum (ER) stress and P300 activity via the XBP1/IRE1 pathway.
Loss of p300 expression is associated with leukemogenesis.
UTX-MLL4-p300 transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
Acetylation-dependent control of global poly(A) RNA degradation by CBP/p300 and HDAC1-HDAC2 has been described.
Data, including data from studies in cells from knockout mice, suggest that Prmt1 activity was necessary for c-Myc binding to acetyltransferase p300 in myeloid cells; Prmt1 inhibition decreases p300 recruitment to c-Myc target promoters and increased Hdac1 recruitment. [Prmt1, protein arginine N-methyltransferase 1; c-Myc = Proto-Oncogene Proteins c-myc; Hdac1 = histone deacetylase 1]
In line with the acetyltransferase activity of p300, H3K27 acetylation was reduced after HDACi and resulted in the formation of heterochromatin in the PTGES1 gene. In conclusion, HDAC activity maintains PTGES1 expression by recruiting p300 to its gene
ARX positively regulates Wnt/ beta-catenin signaling and the C-terminal domain of ARX interacts with the armadillo repeats in beta-catenin to promote Wnt/beta-catenin signaling. In addition, we found BCL9 and P300 also interact with ARX to modulate Wnt/beta-catenin signaling.
2-O, 3-O desulfated heparin inhibited HMGB1 release, at least in part, by direct molecular inhibition of p300 HAT activity.
work shows that helenalin acetate inhibits C/EBPbeta by binding to the N-terminal part of C/EBPbeta, thereby disrupting the cooperation of C/EBPbeta with the co-activator p300.
STAT6 mediates the CT-induced TIM4 expression in DCs. In conclusion, p300 and STAT6 mediate the microbial product CT-induced TIM4 expression in DCs.
Findings indicate that E1a-binding protein (p300) is not required for the normal development or functioning of skeletal muscle.
Hdac3 cooperates with p300 to prime and maintain oligodendrocyte identity
p300 histone acetyltransferase activity is critical for Wnt-dependent palate mesenchymal cell proliferation and migration, both processes that play a significant role in morphogenesis of the palate.
Data indicate that glucose-induced endothelial to mesenchymal transition in vivo and in vitro in the hearts of diabetic mice is possibly mediated by miR-200b and p300.
This gene encodes the adenovirus E1A-associated cellular p300 transcriptional co-activator protein. It functions as histone acetyltransferase that regulates transcription via chromatin remodeling and is important in the processes of cell proliferation and differentiation. It mediates cAMP-gene regulation by binding specifically to phosphorylated CREB protein. This gene has also been identified as a co-activator of HIF1A (hypoxia-inducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. Defects in this gene are a cause of Rubinstein-Taybi syndrome and may also play a role in epithelial cancer.
histone acetyltransferase p300
, histone acetyltransferase
, E1A binding protein p300
, histone acetyltransferase p300-like
, E1A-associated protein p300
, E1A-binding protein, 300kD
, p300 HAT