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Human E1A Binding Protein P300 (EP300) interaction partners

1. results were related to endogenous p63-p300 complex formation and Wnt/beta-catenin-responsive gene regulation by p63 in squamous cell carcinoma lines

2. 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.

3. 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.

4. In which higher levels of P300, but not its homolog CBP.

5. these data imply an important role for p300 in the pathophysiology of diabetes.

6. An analysis in B cells confirms the strong dependency on NAP1-mediated H1 eviction for induction of the silent CD40 gene and further demonstrates that H1 eviction, seeded by activator-p300-NAP1-H1 interactions, is propagated over a CCCTC-binding factor (CTCF)-demarcated region through a distinct mechanism that also involves NAP1

7. SP1 and P300 play an important role during decidualization.

8. 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.

9. 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.

10. P300 may play a key role in ARDS by positively regulating RORgammat transcription.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. 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).

17. 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.

18. 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

19. 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.

20. findings demonstrate that RACK1 is involved in p300/GATA4-dependent hypertrophic responses in cardiomyocytes and is a promising therapeutic target for heart failure

Mouse (Murine) E1A Binding Protein P300 (EP300) interaction partners

1. these data imply an important role for p300 in the pathophysiology of diabetes.

2. Study in a phosphorylation-competent p300 (G442S) knock-in mouse model that ectopically expresses p300 phosphorylation in a homologous site to CREB binding protein Ser436 suggest that a single phosphorylation change in p300 has the capability to modulate hippocampal neurogenesis, Creb binding, and associative fear memory.

3. The data indicate that brachyury mediates acetylated H3K27 recruitment through a physical interaction with p300 during the mouse mesoderm development.

4. 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.

5. Study in mouse model found that liver stiffness activates hepatic stellate cells differentiation into myofibroblasts, which required nuclear accumulation of p300.

6. 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)

7. 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.

8. Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation

9. Data show that LPS induces endoplasmic reticulum (ER) stress and P300 activity via the XBP1/IRE1 pathway.

10. Loss of p300 expression is associated with leukemogenesis.

11. UTX-MLL4-p300 transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.

12. Acetylation-dependent control of global poly(A) RNA degradation by CBP/p300 and HDAC1-HDAC2 has been described.

13. 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]

14. 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

15. 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.

16. 2-O, 3-O desulfated heparin inhibited HMGB1 release, at least in part, by direct molecular inhibition of p300 HAT activity.

17. 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.

18. STAT6 mediates the CT-induced TIM4 expression in DCs. In conclusion, p300 and STAT6 mediate the microbial product CT-induced TIM4 expression in DCs.

19. Findings indicate that E1a-binding protein (p300) is not required for the normal development or functioning of skeletal muscle.

20. Hdac3 cooperates with p300 to prime and maintain oligodendrocyte identity