p300 Human Protein
- Known as:
- p300 Human Protein
- Catalog number:
- 50071
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- p300 Human Protein
Related genes to: p300 Human Protein
- 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: p300 Human Protein
Related articles to: p300 Human Protein
- Urothelial cancer (UC) cells of the luminal subtype exhibit partial, incomplete differentiation towards umbrella cells that line bladder lumen, seen by morphology and gene expression. Differentiation is stalled even though the cells express master transcription factors (MTFs) that drive luminal urothelial differentiation, e.g., FOXA1 and CEBPB, at levels seen in normal differentiated urothelium. We therefore analyzed the FOXA1/CEBPB MTF hub by mass spectrometry. SWI/SNF coactivator complex (CoA) components, e.g., SMARCA4, ARID1A, that read the epigenetic activation mark histone 3 lysine 27 acetylation (H3K27ac) and use ATP-hydrolysis to open chromatin, were the most abundant proteins pulled-down with FOXA1/CEBPB. However, genes for these and other CoA, e.g., CREBBP, EP300 that write H3K27ac, were mutated/deleted in >95% of UCs in clinical series. Also contained in the hub were corepressors (CoR) that erase H3K27ac and close chromatin, e.g., HDAC1, CHD4; genes for these CoR were recurrently gained in UCs. Chromatin analyses showed H3K27ac-centered remodeling was needed to activate umbrella but not constitutively accessible cell growth/division/housekeeping genes. Restoring ARID1A into ARID1A-mutated UC cells using lentiviral transduction, or inhibiting CoR with siRNA or small molecules, activated umbrella genes and terminated replications. In summary, UC-genesis selects for loss- and gain-of-function of CoA and CoR respectively in the urothelial-lineage MTF hub; small molecule CoR-inhibitors are candidate remedies to renew maturation towards terminal differentiated-fates. - Source: PubMed
Publication date: 2026/08/13
Schuerger CarolineBiswas SudiptaNg Kwok PengCardone LisaGu XiaorongGanguly ShinjiniTohme RitaDurmaz ArdaStich MaximilianLindner Daniel JJha BabalMian Omar YSaunthararajah Yogen - Genomic or transcriptomic sequencing guides the precision of cervical cancer (CC) diagnosis; however, the molecular profile of Asian patients remains poorly understood. We established a comprehensive multi-omics cohort comprising 112 tumor-normal adjacent tissue pairs from Chinese CC patients. Our integrated analysis revealed a mutational burden comparable to other populations, with three major mutational signatures primarily attributed to APOBEC-associated, age-associated, and DNA repair-associated biological categories. Multi-omics profiling elucidated the functional consequences of somatic mutations and copy number variations, identifying PIK3CA, EP300, and MPRIP as key driver events. We further uncovered both concordant and discordant activation patterns across cancer-related signaling pathways. Transcriptomic and proteomic analyses nominated cell cycle regulation, epithelial-mesenchymal transition, and LAMC2 as promising diagnostic and therapeutic targets. Comprehensive immune characterization enabled stratification of patients into three major immune phenotypes with varying microenvironmental profiles. This study provides valuable resources and novel insights into the molecular architecture of cervical cancer in the Chinese population, identifying potential biomarkers to guide precision detection and immunotherapy strategies. - Source: PubMed
Publication date: 2026/10/05
Pan TaoZhuang XucuiZhang YaGuo JiyuLi SiZhang CanHan LiliLi FuxiaGao YueyingYu JinyangLi YongshengSun Chaoyang - Alzheimer's disease (AD) arises from converging neurodegeneration and neuroinflammation, yet post-transcriptional mechanisms linking these processes remain poorly defined. Hsa-miR-132-3p, a neuron-enriched microRNA consistently downregulated in AD, has emerged as a candidate integrator of synaptic plasticity and innate immune signaling. Targets of hsa-miR-132-3p were collected from five repositories (miRTarBase v10.0, DIANA-TarBase v9.0, ENCORI v3.0, miRWalk v3.0, miRDB v6.0) and integrated using multiMiR. Functional annotation used ShinyGO v0.81 (KEGG, GO-BP), with immune enrichment via MSigDB Hallmark, ImmPort, and InnateDB. High-confidence targets were defined by overlap with TargetScan conserved predictions and MalaCards AD genes. PPI networks were built with STRING v12.0/MCODE, and transcriptomic validation used GSE5281 hippocampal microarray data. Integration of five repositories identified 5429 non-redundant candidate targets, with significant enrichment in prefrontal cortex and CD33 + myeloid cell signatures (adjusted p < 0.05). Immune analyses highlighted TNFα/NF-κB, IL-6/JAK-STAT3, and interferon signaling overrepresentation. Intersection with TargetScan conserved predictions and MalaCards prioritized a 14-gene module (GSK3B, MAPK1, MAPK3, EP300, FOXO3, PIK3CA, PPP3CA, MAPT, EGR1, NR4A2, SLC30A6, ADCYAP1, SLC6A3, SV2A) defined by the convergence of experimentally supported target annotations, conserved TargetScan predictions, and AD-associated gene annotations. PPI mapping identified MAPK1, MAPK3, EP300, MAPT, and EGR1 as a central interaction module associated with inflammatory signaling and tau-associated processes. Hippocampal transcriptomic analysis provided exploratory evidence of overlap between candidate hsa-miR-132-3p targets and AD-associated differentially expressed genes (KDM4B,CBX3 and MORF4L2). This analysis nominates hsa-miR-132-3p as a candidate post-transcriptional regulator potentially linking neuronal stress, tau pathology, and innate immune signaling in AD. The 14-gene module provides a hypothesis-generating framework for cell-type-resolved experimental validation. - Source: PubMed
Publication date: 2026/10/01
Soltani IsmaelBahia WaelSlaymi ChakerKhemissi WahidRahali NajouaBougatef HajerBaazaoui NarjesFerchichi SalimaAlmawi Wassim Y - CD47 is an innate immune checkpoint that can protect tumor cells from macrophage-mediated clearance, but the regulatory mechanisms underlying its expression in ovarian cancer (OC) remain incompletely understood. Here, we investigated the epigenetic regulation of CD47 expression in OC. Single-cell and spatial transcriptomic analyses indicated preferential CD47 expression in malignant epithelial cells. Integration of publicly available epigenomic datasets revealed a distal regulatory region with enhancer-associated features across ovarian cancer models and HGSOC patient samples. A genome-wide CRISPR-Cas9 screen further implicated PITX2 and EP300 as regulators of CD47 expression. Chromatin immunoprecipitation assay showed PITX2 and EP300 occupancy at candidate enhancer elements within this CD47 regulatory region. Comparative epigenomic analyses suggested that features of this regulatory landscape are also present in fallopian tube epithelial cells and become more prominent in OC. suTogether, these findings support a PITX2-EP300 regulatory axis associated with CD47 expression and provide evidence for its potential contribution to tumor immune evasion. - Source: PubMed
Publication date: 2026/09/10
Mishra Alok KBiswas TanayRoy AnjanBanday ShahidKatiyar ArpitSharma AnshulLi RuiZhu Lihua JulieMalonia Sunil KAteeq Bushra - Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system characterized by progressive neuroinflammation and demyelination. Increasing evidence suggests that the gut microbiota contributes to MS pathogenesis through bidirectional gut-brain interactions; however, the underlying mechanistic framework remains incompletely defined. - Source: PubMed
Publication date: 2026/09/26
Wang JinxiZheng FangxiongZhang YuchenLu Zhongxin