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Human p300 Protein expressed in Insect cells (Sf9) - ABIN2720219
Martinez, Abe, Hong, Molyneux, Yarnell, Löhr, Driever, Acosta, Arcos-Burgos, Muenke: An Ultraconserved Brain-Specific Enhancer Within ADGRL3 (LPHN3) Underpins Attention-Deficit/Hyperactivity Disorder Susceptibility. in Biological psychiatry 2016
Our data show that the hyperacetylation of Tau by p300 histone acetyltransferase (HAT) disfavors liquid-liquid phase separation , inhibits heparin-induced aggregation, and impedes access to LLPS-initiated microtubule assembly
EP300 variants are associated with Rubinstein-Taybi syndrome.
High P300 expression is associated with recurrence in prostate cancer.
Data generated with primary human hepatic stellate cells (HSC) supports that stiffness-mediated HSC activation requires p300.
The histone acylation activity of p300 can be activated by pre-existing lysine crotonylation through a positive feedback mechanism.
epigenomic profiling of clear cell renal cell carcinoma (show MOK Proteins) (ccRCC) establishes a compendium of somatically altered cis (show CISH Proteins)-regulatory elements, uncovering new potential targets including ZNF395 (show ZNF395 Proteins). Loss of VHL (show VHL Proteins), a ccRCC signature event, causes pervasive enhancer malfunction, with binding of enhancer-centric HIF2a (show EPAS1 Proteins) and recruitment of histone acetyltransferase p300 at preexisting lineage-specific promoter-enhancer complexes
Histone acetyltransferase EP300 is necessary for the transcription factor SOX2 (show SOX2 Proteins) activity in basal cells, including for induction of the squamous fate. EP300 copy number gains are common in squamous cell carcinoma SQCCs, including lung cancer SQCC cell lines.
High expression of EP300 is associated with colorectal cancer.
Transcriptional coactivator p300 gene polymorphism correlates with the development and advancement of diabetic kidney disease. Additionally, the SIRT1 (show SIRT1 Proteins) gene collaborates with the p300 gene and participates in promoting albuminuria in type 2 diabetes mellitus patients.
These results reveal a novel RTK-AKT (show AKT1 Proteins)-p300-ADA3 (show TADA3 Proteins) signaling pathway involved in growth factor-induced cell cycle progression.
Study in mouse model found that liver stiffness activates hepatic stellate cells differentiation into myofibroblasts, which required nuclear accumulation of p300 (show NOTCH1 Proteins).
Data (including data from studies in knockout and transgenic mice) suggest that Ep300 and Crebbp (show CREBBP Proteins) 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 (show CREBBP Proteins) = CREB binding protein (show CREBBP Proteins))
Here the authors report a lipopolysaccharide-induced NFkappaB enhanceosome in which TonEBP (show NFAT5 Proteins) is required for the recruitment of p300 (show NOTCH1 Proteins). Increased expression of TonEBP (show NFAT5 Proteins) enhances the NFkappaB activity and reduced TonEBP (show NFAT5 Proteins) expression lowers it.
Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 (show CREBBP Proteins) sequentially shape dynamic enhancer landscapes during cell differentiation
Data show that LPS (show TLR4 Proteins) induces endoplasmic reticulum (ER) stress and P300 (show NOTCH1 Proteins) activity via the XBP1 (show XBP1 Proteins)/IRE1 (show ERN1 Proteins) pathway.
Loss of p300 (show NOTCH1 Proteins) expression is associated with leukemogenesis.
UTX (show KDM6A Proteins)-MLL4-p300 (show NOTCH1 Proteins) 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 (show CREBBP Proteins) and HDAC1-HDAC2 (show HDAC1 Proteins) has been described.
Data, including data from studies in cells from knockout mice, suggest that Prmt1 (show PRMT1 Proteins) activity was necessary for c-Myc (show MYC Proteins) binding to acetyltransferase p300 (show NOTCH1 Proteins) in myeloid cells; Prmt1 (show PRMT1 Proteins) inhibition decreases p300 (show NOTCH1 Proteins) recruitment to c-Myc (show MYC Proteins) target promoters and increased Hdac1 (show HDAC1 Proteins) recruitment. [Prmt1 (show PRMT1 Proteins), protein arginine N-methyltransferase 1 (show PRMT1 Proteins); c-Myc (show MYC Proteins) = Proto-Oncogene (show RAB1A Proteins) Proteins c-myc (show MYC Proteins); Hdac1 (show HDAC1 Proteins) = histone deacetylase 1 (show HDAC1 Proteins)]
In line with the acetyltransferase activity of p300 (show NOTCH1 Proteins), H3K27 acetylation was reduced after HDACi and resulted in the formation of heterochromatin in the PTGES1 gene. In conclusion, HDAC (show HDAC3 Proteins) activity maintains PTGES1 expression by recruiting p300 (show NOTCH1 Proteins) to its gene
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