EP300 Mouse Monoclonal Antibody
- Known as:
- EP300 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002033-M02
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- EP300 Mouse Monoclonal Antibody
Related genes to: EP300 Mouse Monoclonal 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 Mouse Monoclonal Antibody
Related articles to: EP300 Mouse Monoclonal Antibody
- Radiation-induced enteritis (RIE) is a severe, dose-limiting toxicity of cancer radiotherapy lacking mechanism-based therapies. While the gut microbiome regulates radiation injury, harnessing it therapeutically remains challenging. Here, we show that the natural product β-elemene protects against RIE through a synergistic mechanism coordinating host and microbial responses. β-elemene directly rescues the radiation-disrupted interaction between the lactate transporter MCT1 and its chaperone CD147 in intestinal epithelial cells, priming them for enhanced lactate uptake. Concurrently, β-elemene selectively enriches for Lactobacillus gasseri, increasing intestinal lactate production. The convergence of host priming and elevated lactate availability triggers a metabo-epigenetic cascade. Specifically, lactate drives the lactylation of the chromatin-associated protein RBBP4, which in turn recruits EP300 to activate the transcription of essential DNA damage repair genes. We further identify EP300 as a lactyl-transferase, establishing a self-amplifying positive feedback loop that robustly enhances the repair signal. Our findings delineate a complete drug-microbe-metabolite-epigenome axis, establishing a 'prime-and-fuel' therapeutic strategy where a single agent orchestrates inter-kingdom communication to promote tissue regeneration. - Source: PubMed
Publication date: 2026/05/27
He JianchengBao JiapengDeng ShukangZang WeijieYan HaomingZhao ZihaoZhang GuangzeLiu RuiqingChen JunjieHu YilinXue Wanjiang - Synovial sarcoma (SS) is a rare and aggressive soft tissue malignancy characterized by t(X;18)(p11.2;q11.2) translocation, which results in the SYT-SSX fusion gene. SS exhibits cancer stem cell-like properties that contribute to its invasiveness. Recent evidence implicates microRNA-29b (miR-29b) could regulate TGF-β pathway and its downstream gene EP300 may be involved in these traits. Bioinformatics tools (miRDB, TargetScan, and miRanda) were used to predict the interaction between miR-29b-5p and EP300, which was validated via dual-luciferase reporter assays and RNA-binding protein immunoprecipitation. The expression levels of miR-29b-5p and EP300, along with those of cancer stem cell markers, LIF-LIFR signaling, and Ki-67 proliferation indices, were analyzed in SS tissues, parental cells, and spheroid cells. Spheroids derived from SW982 and SSX1 cells cultured in serum-free suspension presented elevated levels of cancer stem cell markers and increased proliferation, migration, and invasion capacities, particularly SYT-SSX1-derived spheroids. Compared with parental cells, spheroids presented reduced miR-29b-5p expression and increased EP300 expression. The overexpression of miR-29b-5p suppressed spheroid formation; stemness marker expression; and cell proliferation, migration, and invasion, whereas its inhibition had the opposite effect. Compared with individual silencing, co-silencing of miR-29b-5p and EP300 further attenuated cancer stem cell-like traits, underscoring their regulatory interplay. In conclusion, miR-29b-5p may suppresses cancer stemness and aggressiveness in SS to some extent by targeting EP300, with a relatively more pronounced effect in SSX1 cells. Preliminarily these fundings suggest that miR-29b-5p-mediated modulation of EP300 and the TGF-β signaling pathway may provide a potential research data for synovial sarcoma studies. - Source: PubMed
Publication date: 2026/05/26
Xu HuiLingDong ShuangShuangZhang ZhenWang NingXie MingYuPang LiJuanLi FengQi Yan - Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development. - Source: PubMed
Publication date: 2026/05/26
Tang QianLian ChenHan XinyanZhang XuhanWang ZihanWang BoyuZhu TaoyuLin XinruiWang XiaoleiXu YapingXiao ManyuWang ZijinLi JunmingChen SilinWang YunzeLiu YufeiLi SongsongShen ZuolinLu XiHan XueqiZhou YiluXiao MingyangRan JiayiCao XiaoranXu XinyiSámano-Sánchez HugoRodríguez AlfredoWang LianChen ShuifangXu ZhanyuZhang ShirongYang NuoTang YongLiu Jian - Liver fibrosis is a shared pathological phenotype of chronic liver diseases of diverse etiologies, including viral hepatitis, alcohol-associated liver disease and metabolic dysfunction-associated steatohepatitis (MASH), as well as cholestatic liver diseases such as primary biliary cholangitis and primary sclerosing cholangitis, and may progress to cirrhosis, hepatic decompensation and hepatocellular carcinoma. Despite advances in etiological treatments, effective therapies for established fibrosis remain limited. Increasing evidence indicates that liver fibrosis is a dynamic and potentially reversible process. The Wnt/β-catenin pathway is central to both liver regeneration and fibrogenesis and has traditionally been interpreted in terms of quantitative activation. Recent studies demonstrate that β-catenin-dependent transcription is qualitatively regulated by its nuclear coactivators, CREB-binding protein (CBP) and p300. CBP- and p300-associated transcriptional programmes exert distinct biological effects, promoting fibrogenic or regenerative states, respectively. These findings support a broader conceptual framework in which liver fibrosis can be viewed as a transcriptionally regulated and potentially reversible pathological state. In this review, we first summarize the molecular basis of canonical Wnt/β-catenin signalling and its transcriptional regulation by CBP and p300. Then, we discuss the pathophysiological relevance of CBP- versus p300-dependent β-catenin transcription in liver fibrosis of various etiologies, including cholestatic injury, and review experimental and early clinical evidence suggesting that selective modulation of CBP-associated transcription may promote early functional recovery, potentially preceding measurable regression of fibrotic burden. We close by considering implications for clinical trial design and the importance of function-oriented endpoints in antifibrotic drug development. - Source: PubMed
Kimura KiminoriKohara Michinori - The acetylation level of XRCC6 is significantly decreased in clinical breast cancer tissues compared with paracancerous tissues; however, the relationship between this alteration and the occurrence and development of breast cancer remains unclear. - Source: PubMed
Publication date: 2026/05/08
Yin JieLiu JiaxingHe MeiruiXiao TangXiang WenjuanSheng RuxiaZhao HaifangHuang XinyueXu ShengZhou YongLiu JunfengHeng RuijuanHe XiaoyingWang YunxiangSong YuQi Pan