Monoclonal Mouse EP300 Antibody
- Known as:
- Monoclonal Mouse EP300 Antibody
- Catalog number:
- abx000050
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Monoclonal Mouse EP300 Antibody
Related genes to: Monoclonal Mouse EP300 Antibody
- Gene:
- EP300 NIH gene
- Name:
- E1A binding protein p300
- Previous symbol:
- -
- Synonyms:
- p300, KAT3B
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-31
- Date modifiied:
- 2015-09-11
Related products to: Monoclonal Mouse EP300 Antibody
Related articles to: Monoclonal Mouse EP300 Antibody
- Super enhancers (SEs) are involved in regulating cell identity and lineage‑specific gene expression, and drive cancer‑associated gene expression. The transcription factor Kruppel‑like factor 6 (KLF6) promotes the growth and progression of clear cell renal cell carcinoma (ccRCC), with its high expression driven by one of the strongest SEs in ccRCC. However, the mechanisms that establish and maintain SE activity, particularly the roles of epigenetic regulators bromodomain-containing 4 (BRD4) and p300, remain poorly understood. This study investigated the roles of BRD4 and p300 in modulating SE activity. The effects of JQ1‑mediated BRD4 and A‑485‑mediated p300 inhibition were assessed using cell viability and colony formation assays. Reverse transcription‑quantitative (q)PCR and ChIP‑qPCR were employed to evaluate the impact of BRD4 and p300 inhibition, as well as CRISPR‑mediated deacetylation of individual constituent enhancers, on expression and SE activity. Chemical inhibition of BRD4 and p300 significantly reduced ccRCC cell viability and colony formation, and decreased KLF6 expression and levels of acetylation at lysine 27 of histone H3 (H3K27ac) at enhancer regions SE_1, SE_2 and SE_3, suggesting decreased chromatin accessibility. On the other hand, deacetylation of SE_1 using dead Cas9 fused to histone deacetylase 3, led to downregulation, which was associated with decreased H3K27ac signals at this region. The present results demonstrated that BRD4 and p300 are key for maintaining SE activity and driving high expression in ccRCC. However, deacetylation of individual enhancer regions using CRISPR was insufficient to fully suppress transcription, emphasizing the robustness of the KLF6 SE and its modular role in sustaining high expression. Overall, the present study deepens the understanding of growth‑promoting KLF6 transcriptional networks in ccRCC and offers insights to support the development of diagnostic or therapeutic strategies. - Source: PubMed
Publication date: 2026/04/17
Zamberi Nurul Nadia MohamadAbuhamad Asmaa YYusuf Siti Nur Hasanah MohdRahman Nur Qurratu Athirah AMohtar Mohamad AimanuddinSyafruddin Saiful Effendi - Parkinson's disease (PD) is the second most common neurodegenerative disorder. Although the etiology of idiopathic PD is unclear, recessive loss-of-function mutations in PARK7/DJ-1 cause familial early-onset PD, which mirrors key features of the idiopathic form. In this study, we ablate PARK7/DJ-1 via CRISPR-Cas9 from the human neuronal cell line, SH-SY5Y. Subsequently, RNA sequencing and the DESeq2 toolkit were utilized to identify 5468 differentially expressed genes (DEG) between PARK7/DJ-1 knockouts and control SH-SY5Y cells. Three genes from each of the top 10 upregulated and downregulated gene lists were selected and confirmed via RT-PCR. Differentially expressed gene lists were run through the WebGestalt functional enrichment analysis toolkit to identify enriched gene ontology (GO) terms. Among the top significantly enriched GO biological process terms include terms related to synaptic transmission (downrgulated DEG) and development (upregulated DEG). Differentially expressed genes were run through the STRING database to predict protein-protein interactions (PPI). A highly significant PPI enrichment was observed (p < 1.0e-16). To gain insight into what could potentially be driving the observed expression changes, we performed an iRegulon analysis within Cytoscape to identify potential upstream transcription factors. The top transcriptional factors identified for driving downregulated genes was REST, while EP300 was identified as the top candidate driving upregulated genes. Our results indicate that loss of DJ-1 in human neuronal cells leads to dysregulation of networks of connected genes and pathways that are implicated in neurodegenerative disease as well as neuronal function. - Source: PubMed
Publication date: 2026/04/14
Gock NathanKim GraceMorin TessaYoung Markus AMahal AmarKostka JuliaBeischlag Timothy VLee Frank J S - Recently, a distinct, bland spindle cell neoplasm with rhabdomyoblastic phenotype, and VGLL3 rearrangement has been described. These tumors have a striking predilection for the head and neck area and so far, followed an indolent course. It remains unclear whether these tumors are best classified as true rhabdomyosarcomas. There are 11 reports of such tumors with limited follow-up. Here, we report an additional case with local recurrence, long-term follow-up and spatial profiling. The tumor occurred in the right buccal mucosa/oral commissure of a 47-year-old man. On clinical examination, the mass was firm, measuring ~1.5 cm. Biopsy and subsequent wedge excision were performed. Histologically, the tumor was composed of bland, small, spindle to ovoid cells, arranged in short fascicles and vaguely storiform architecture. The tumor cells diffusely infiltrated into skeletal muscle. There was a background of inflammatory cells including small lymphocytes and histiocytes. Neoplastic cells were positive for SMA, demsin, PAX7, myogenin and MyoD1. Whole transcriptome sequencing revealed a TCF12::VGLL3 fusion. Digital spatial profiling (DSP) identified pan-AKT expression, differential expression in the MAPK pathway, and revealed that the tumor attracted a dense T-cell rich inflammatory infiltrate. The patient had a lesion in the same location 6 years prior that underwent incisional biopsy, showed intense inflammatory infiltrate, and was interpreted as benign. FISH for VGLL3 on this tissue was positive for rearrangement. No additional adjuvant treatment was given, and the patient is alive without disease, 8 months after the major resection. Long term follow-up of 6 years with only local recurrence lends further support to the notion that these neoplasms are a class of indolent/low-grade rhabdomyoblastic tumors that are biologically and clinically distinct from fully malignant spindle cell rhabdomyosarcomas. - Source: PubMed
Dashti Nooshin KChakraborty DebopriyaSadanandappa Madhumala KDehner Carina AZhang Paul JPaydarfar Joseph ATafe Laura J - While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are a cornerstone of therapy for advanced -mutant non-small cell lung cancer (NSCLC), resistance remains a major clinical challenge. The genomic landscape of early-stage (ES) -mutant NSCLC and its evolution to advanced-stage (AS) disease is not fully understood. This study aimed to characterize the molecular disparities between ES and AS -mutant NSCLC and to identify genomic alterations associated with EGFR-TKI treatment outcomes. - Source: PubMed
Publication date: 2026/02/26
Yoon DayoungLee Ji WonCho Byoung ChulKang Eun JooKim Jung SunLim TaekyuYi Seong YoonKim Yu JungAhn Mi SunKim Young SaingPark Ji HyunLim SeungtaekPark Hyung SoonCho Jang HoJang ByunghyunLee Ji YoonKim JiwonHong JisooKoo HarimChung SeokShin Sang WonKim Yeul HongSa Jason KChoi Yoon Ji - Curcumin, a natural polyphenolic compound known for its antitumor efficacy, has been shown to modulate glycolytic pathways in various cancers. However, its specific role and underlying mechanism in oral squamous cell carcinoma (OSCC) remain insufficiently explored. This study systematically investigated the impact of curcumin on glycolysis in OSCC cells, with particular focus on EP300, a key epigenetic regulator, as a target of curcumin’s action. Human oral squamous cell carcinoma cell lines (UM-SCC-1 and HSC-3) and normal human oral keratinocytes (HOK) were treated with curcumin at various concentrations. Cell proliferation, clonogenic ability, and migration were assessed using CCK-8, colony formation, and wound-healing assays, respectively. Glycolytic activity was evaluated by measuring glucose uptake and lactate production. An EP300-overexpressing UM-SCC-1 cell line was established via plasmid transfection. Protein-protein interaction (PPI) network analysis through the STRING database identified potential EP300-regulated glycolytic enzymes. Expression levels of EP300 and key glycolytic markers (PKM2, LDHA, GLUT1) were quantified using qRT-PCR and Western blot. Curcumin significantly inhibited proliferation, clonogenic growth, and migration of OSCC cells (UM-SCC-1 and HSC-3) in a concentration-dependent manner. Curcumin treatment markedly reduced glucose uptake and lactate production in OSCC cells, indicating effective suppression of glycolytic activity. At the molecular level, Curcumin downregulated EP300 expression. EP300 overexpression enhanced glycolytic activity and increased the expression of key glycolytic enzymes, including PKM2, LDHA, and GLUT1, and partially reversed the inhibitory effects of curcumin on glycolysis and enzyme expression. Bioinformatic analysis confirmed interactions between EP300 and these glycolytic enzymes. Curcumin suppresses glycolysis in OSCC by modulating EP300 expression and downregulating key glycolytic enzymes such as PKM2, LDHA, and GLUT1. These findings are consistent with curcumin’s potential role as a metabolic modulator in OSCC. - Source: PubMed
Publication date: 2026/04/07
Tan WanrongZhang ChaoHan LiFu HaoxuanMao ZhouhongZhang YonghengLiu YingLi LihuaYu Jie