p300 EMSA Probe Set
- Known as:
- p300 EMSA Probe Set
- Catalog number:
- AY1133P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- p300 EMSA Probe Set
Related genes to: p300 EMSA Probe Set
- 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 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: p300 EMSA Probe Set
- 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
Baranov EstherAmeline BaptisteBerthold RuthPerry Kyle DTorres-Mora JorgeMaclean FionaAbrahao-Machado Lucas FMichal MichaelKerr Darcy ALu LiangHou TieyingMalik FaizanGoldfaden JoshuaPrasad JoanneGestrich CatherineStelow EdwardFanburg-Smith Julie CLeGallo RobinZadeh SaraHaglund de Flon FelixZhang Paul JHartmann WolfgangMiele EvelinaStejskal VáclavAlaggio RitaAgaimy AbbasNielsen Gunnlaugur PeturDemicco Elizabeth GBaumhoer DanielDehner Carina A - Trained immunity is defined as the epigenetic and metabolic reprogramming of innate immune cells, conferring enhanced or diminished responsiveness to secondary challenges following initial stimulation. Immune tolerance represents the state of immunological unresponsiveness to self-antigens or innocuous foreign antigens. Systems pharmacology approaches have emerged as essential tools for understanding and modulating these complex immunological processes. In this mini-review, we evaluate quantitative systems pharmacology (QSP) approaches which are predominantly based on ordinary differential equation (ODE) frameworks and artificial intelligence (AI)/machine learning (ML) applications in the context of trained immunity and immune tolerance. QSP models enable in silico clinical trials, thereby accelerating drug development and supporting cost-effective therapeutic decision-making. Recent advances have identified histone lactylation, particularly H3K18la, as a central epigenetic mark linking metabolic rewiring to long-term innate immune memory, revealing novel pharmacological targets including LDHA, EP300, and ACAT2. ML algorithms integrated with explainable AI frameworks have facilitated biomarker discovery and therapeutic target identification. Digital twin technology holds considerable promise for developing personalized immunomodulatory strategies. This review highlights the translational potential of systems pharmacology tools in pharmacological targeting of trained immunity and tolerance, emphasizing the convergence of computational modeling with precision medicine approaches. - Source: PubMed
Publication date: 2026/04/21
Kırboğa Kevser KübraRudrapal Mithun - Hepatocellular carcinoma (HCC), a malignancy driven by multifaceted genetic and epigenetic mechanisms, is the leading cause of cancer deaths worldwide. Long non-coding RNAs (lncRNAs), particularly super-enhancer-associated lncRNAs (SE-lncRNAs), have emerged as critical regulators of tumorigenesis. - Source: PubMed
Publication date: 2026/05/13
Ye WeidongXiao JunyuanLi JiaxinYang ChengLi ChunlaiXi ZhifengCheng Zhuoan - Rubinstein Taybi syndrome (RSTS), a rare congenital disease, is caused by mutations in lysine acetyl transferase type 3 (KAT3) genes, EP300 and CREBBP. Many of the tissues affected in RSTS are derived from the neural crest (NC). Hence, we proposed that NC development would be perturbed in RSTS. - Source: PubMed
Publication date: 2026/05/11
Verma ShwetaDalabehera SujitGowda SubhashChandrasekaran KoushikaSingh DayanidhiPrasher BhavanaBapat SharmilaRamalingam SivaprakashSachidanandan Chetana