Ask about this productRelated genes to: 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: EP300 antibody
Related articles to: EP300 antibody
- LncRNA HOXB-AS3 has been shown to exert oncogenic effects in various malignancies. However, its specific role in gastric cancer (GC) remains largely unknown. This study addressed the expression profile and clinical relevance of HOXB-AS3 in GC. Moreover, we dissected its downstream regulatory circuitry in a cell model. - Source: PubMed
Publication date: 2026/05/19
Ding YushuangZhang LihongXu YuanCen MeiniLi Pengfei - Renal fibrosis is a final common pathological outcome of chronic kidney disease, and EP300 has been implicated in fibrogenic responses. However, the mechanism that regulates EP300 protein levels in renal proximal tubule epithelial cells remains unclear. Here, we investigated whether PPM1M regulates EP300 protein levels and modulates TGF-β-induced fibrogenic responses. In HK-2 cells, TGF-β increased protein levels of EP300, and PPM1M overexpression reduced TGF-β-induced EP300 accumulation. The interaction between EP300 and PPM1M was assessed by proximity ligation assays, and the results showed that this interaction was diminished following TGF-β treatment. Furthermore, immunoprecipitation assays using in vitro-translated proteins supported a direct interaction between EP300 and PPM1M. Overexpression of PPM1M in HK-2 cells reduced the TGF-β-induced increases in EP300 phosphorylation at Ser1834 and total EP300 protein levels. Functionally, PPM1M attenuated TGF-β-induced EMT and fibrosis-associated transcriptional changes in HK-2 cells. Consistent with these findings, protein levels of EMT- and fibrosis-related markers were decreased by PPM1M overexpression, and TGF-β-induced spindle-like morphological changes were significantly attenuated. Analysis of a human chronic kidney disease dataset showed that PPM1M transcript levels were reduced, and PPM1M expression was decreased in the unilateral ureteral obstruction model, where EP300 expression was increased. Together, these findings suggest that PPM1M may act as a negative regulator of EP300 phosphorylation and protein levels, thereby modulating TGF-β-induced EMT and fibrogenic responses in proximal tubular epithelial cells. - Source: PubMed
Publication date: 2026/05/17
Kim HyunsikLee Sun-HoKwon Jae-HwanByun SeungheeKim HyunseungLee DonggueCha SeungheonPark Soo-YeonYoon Ho-Geun - To elucidate potential molecular intersections between ribavirin and Major Depressive Disorder (MDD) and to generate testable hypotheses regarding neuropsychiatric safety and mechanism of action. - Source: PubMed
Publication date: 2026/05/11
Chen ChengWang TianchengFang CancanWang XiaoyueShen TingGao Song - Bevacizumab, a monoclonal antibody targeting Vascular Endothelial Growth Factor (VEGF), is a cornerstone therapy for ovarian cancer (OC). However, acquired resistance to bevacizumab remains a major clinical challenge. Metabolic reprogramming in the tumor microenvironment, particularly lactate-driven lactylation modifications, has been implicated in drug resistance; however, the specific mechanisms underlying bevacizumab resistance are poorly understood. This study identifies Enolase 1 (ENO1) lactylation as a key driver of drug resistance through the integration of lactylation proteomics in patient samples, functional validation in cell lines and in vivo models Patient-Derived Xenograft (PDX), zebrafish, and chicken Chorioallantoic Membrane (CAM)). We observed significantly elevated pan-lactylation in bevacizumab-resistant OC tissues, correlating with enhanced angiogenesis and poor prognosis. Mechanistically, alanyl-tRNA synthetase 1 (AARS1) mediated lactylation of ENO1 at lysine 71 (K71) augmented lactate synthesis and promoted histone lactylation marks (Lysine lactylation of histone H3 at lysine 9 (H3K9la) and Lysine Lactylation of Histone H3 at Lysine 14 (H3K14la)). This epigenetic reprogramming upregulated the transcription of the angiogenic factor Endothelial cell-specific molecule 1 (ESM1), establishing a positive feedback loop for ENO1 expression. Secreted ESM1 stabilized the transcription factor YY1 in endothelial cells by competitively inhibiting Smurf2-mediated ubiquitination, leading to YY1-dependent recruitment of E1A Binding Protein p300 (EP300) and Histone H3 Lysine 27 (H3K27) acetylation at the B-cell lymphoma 2-related protein A1 (BCL2A1) promoter. This cascade enhanced endothelial cell survival and angiogenesis, ultimately fostering resistance to bevacizumab. Our findings reveal a metabolic-epigenetic axis centered on ENO1 K71 lactylation that perpetuates resistance to bevacizumab, highlighting its potential as a therapeutic target to restore bevacizumab efficacy in OC. - Source: PubMed
Publication date: 2026/05/07
Zeng TianWang QianqianLi LeiTan XiongjinHe JingLiu YanWang XiaodongHe RongfangDing GoupingZeng XinyiTang XingChen XunHuang HaoLi Yukun - A rare spindle cell tumor with skeletal muscle phenotype, male predilection, exclusive involvement of the head and neck region, particularly the tongue, and a suggested indolent course has been previously reported as VGLL3-rearranged spindle cell rhabdomyosarcoma (SRMS). We report 18 cases with extended clinical follow up, detailed molecular results, and methylation profiling. Tumors occurred in 5 females, 12 males, and 1 patient of unknown sex with median age of 58 years (range: 22-71). Tumors involved tongue (n=13), lower lip (2), retropharyngeal region (n=1), thyroid/parathyroid (n=1), and palatine tonsil (1) with median size of 1.2 cm. Treatment details (15 patients) revealed that 13 patients underwent excision only, while 1 patient underwent adjuvant chemotherapy and 1 adjuvant radiation therapy. Follow-up (11 patients) showed no local recurrence or metastases. At last follow-up (median: 45 months, range: 1- 326 months) all patients were alive without evidence of disease. Histologically, tumors showed spindled to histiocytoid cells arranged in a fascicular, storiform or haphazard architecture with variably collagenous stroma, rounded to infiltrative borders and often diffusely growing through skeletal muscle, adipose tissue, and entrapped nerves. Necrosis was consistently absent with a median mitotic rate of 1/10 HPFs (range: 0-7/10). By immunohistochemistry, tumors diffusely expressed desmin (n=18), multifocal MyoD1 (n=15) and/or myogenin (n=12), and sometimes SMA (n=7). Molecular testing revealed EP300::VGLL3 (n=6), TCF12::VGLL3 (n=5), and PPARGC1A::VGLL3 (n=1) fusions with VGLL3-rearrangement by fluorescence in situ hybridization (FISH) in 3 cases. One archival tumor failed molecular and methylation testing despite multiple attempts, likely due to decreased DNA/RNA integrity, yet was included given classic morphological features. Methylation data (n=12) revealed all but 1 tumor to form a distinct group separate from other fusion-driven rhabdomyosarcomas, including 5 infantile/congenital SRMS. We describe a well-characterized series of these rare tumors with extended follow-up data confirming lack of progression or recurrence. Further, our DNA methylation profiling data supports these tumors to form a distinct cluster, regardless of VGLL3 fusion partner, and separate from morphologic mimics and other fusion-driven SRMS, including 5 cases of congenital SRMS. We propose that these neoplasms may be better classified as VGLL3-rearranged spindle cell rhabdomyoblastic tumors to reflect their indolent behavior and to prevent overtreatment. - Source: PubMed
Publication date: 2026/05/12
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