EP300 Mouse Monoclonal Antibody
- Known as:
- EP300 Mouse Monoclonal Antibody
- Catalog number:
- BIN-002033-M01
- Product Quantity:
- 0.1mg
- 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
- Antipsychotic-induced weight gain (AIWG) is a major clinical concern, affecting approximately 30% of patients. Clinical predictors explain only part of AIWG risk. Genetic and molecular variations are hypothesized to contribute to susceptibility. The purpose of this review is to summarize recent results to identify replicated and novel findings. - Source: PubMed
Publication date: 2026/07/21
Kronenbuerger MartinYoshida KazunariLi Pei YuanTavakoli EmytisMagarbeh LeenElsheikh Samar S MGorbovskaya IlonaZai Clement CFleischmann RobertZai GwynethKloiber StefanKennedy James LMüller Daniel JTiwari Arun K - N6-methyladenosine (m6A) RNA modification regulates pulmonary inflammation, yet the precise function of the m6A reader IGF2BP2 in acute lung injury (ALI) remains elusive. Here, we reveal that IGF2BP2 and global m6A levels are significantly upregulated in lipopolysaccharide (LPS)-induced ALI. Prophylactic genetic silencing or pharmacological inhibition of IGF2BP2 robustly mitigated pulmonary hyperinflammation, epithelial apoptosis, and pathological tissue damage. Mechanistically, transcriptome profiling identified MARCKSL1 as a direct downstream target. We demonstrate that IGF2BP2 binds and post-transcriptionally stabilizes MARCKSL1 mRNA in a partially METTL3/m6A-dependent manner. Elevated MARCKSL1 subsequently drives NF-κB p65 nuclear translocation and activation, fueling the inflammatory cascade. Strikingly, we trace this IGF2BP2 dysregulation upstream to inflammatory metabolic reprogramming: elevated alveolar glycolysis drives lactate accumulation, which triggers EP300-mediated histone lactylation (H3K18la) at the IGF2BP2 promoter to activate its transcription. Pharmacological manipulation of glycolysis confirmed this metabolic-epigenetic coupling. Collectively, our findings decipher a novel H3K18la/IGF2BP2/MARCKSL1 signaling cascade that integrates metabolic reprogramming with m6A epitranscriptomics in ALI, highlighting IGF2BP2 as a promising target for preventive intervention in airway epithelial inflammation. - Source: PubMed
Publication date: 2026/07/17
Peng YangdiZhang JunyaoYang YangLin YangjingCai PiaopiaoWu Peiliang - Curcumin exhibits significant antitumor activity, inhibiting proliferation, angiogenesis, invasion, and metastasis, highlighting its potential for cancer treatment. However, its mechanisms in Laryngeal and Pharyngeal Carcinoma remain unclear. Therefore, this study aims to elucidate these mechanisms through in vitro and in vivo experiments. - Source: PubMed
Publication date: 2026/07/13
Lei JixiangTang XianyunLin YuanchaoYang RuiMa Zhiyue - E1A-binding proteins p300 (EP300) and CREB-binding protein (CBP) are two homologous multidomain enzymes that have emerged as promising therapeutic targets in oncology. Recent drug discovery efforts have yielded degraders that target EP300/CBP by engaging either the bromodomain or the histone acetyltransferase (HAT) domain, with the latter potentially leading to preferential or selective degradation of one paralog. Building on a potent proline-based EP300/CBP HAT domain inhibitor, we designed, synthesized, and characterized a series of novel HAT-targeting and cereblon-recruiting proteolysis-targeting chimeras (PROTACs). In particular, compound was identified as a PROTAC that promotes preferential degradation of EP300 over CBP, highlighting the potential of HAT domain engagement to modulate paralog selectivity. Functional studies in REH cells showed that preferential EP300 degradation by resulted in impaired proliferation, G1 cell cycle arrest, and induction of apoptosis. Thus, HAT-targeting degrader provides a promising foundation for further optimization toward therapeutic applications in EP300-dependent malignancies. - Source: PubMed
Publication date: 2026/06/08
Tan KathrinVogt MelinaSchaal KaterinaSwapna SwapnaGeiger Thomas MDressel InaNowak Radosław PBhatia SanilHansen Finn K - Geroprotection aims at extending healthspan by delaying age-associated pathologies. Polyamines including spermine and spermidine are interconvertible metabolites whose longevity-promoting effects have traditionally been attributed to autophagy induction. In addition, recent evidence identifies spermine as an endogenous Fe chelator that suppresses ferroptosis, thereby complementing the autophagy-inducing activity of spermidine. Indeed, spermidine inhibits EP300 acetyltransferase activity and supports hypusination-dependent activation of TFEB, both leading to autophagy. However, enhanced autophagic flux may increase susceptibility to ferroptosis through ferritinophagy and lipid remodeling. In parallel, polyamine catabolism generates HO and acrolein, both of which facilitate lipid peroxidation and ferroptotic demise. The discovery that spermine directly chelates redox-active Fe closes a conceptual gap by explaining how polyamine supplementation can promote longevity while avoiding excessive ferroptotic cell loss. Multiple lines of evidence including metabolomics, isotope tracing, cell-free lipid peroxidation systems, Fe-binding biophysics, mass spectrometry, Raman spectroscopy, nuclear magnetic resonance and disease models demonstrate that spermine limits labile iron and ferroptosis. Together, these findings support a unified model in which spermidine-driven autophagy and spermine-mediated ferroptosis inhibition cooperate to preserve tissue homeostasis and healthspan. - Source: PubMed
Publication date: 2026/07/03
Madeo FrankCarmona-Gutierrez DidacKroemer Guido