PRMT5 Assay Kit_Luminescent
- Known as:
- PRMT5 Assay Kit_Luminescent
- Catalog number:
- 52002L
- Product Quantity:
- 100 reactions
- Category:
- Peptides
- Supplier:
- BPS Bioscience
- Gene target:
- PRMT5 Assay Kit_Luminescent
Related genes to: PRMT5 Assay Kit_Luminescent
- Gene:
- PRMT5 NIH gene
- Name:
- protein arginine methyltransferase 5
- Previous symbol:
- HRMT1L5, SKB1
- Synonyms:
- SKB1Hs
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-18
- Date modifiied:
- 2017-12-15
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- Homozygous deletion of 9p21, containing CDKN2A/B and MTAP (CMdel), underlies emerging therapeutic strategies including PRMT5/MAT2A inhibition. The clinicogenomic context and treatment outcomes of CMdel in NSCLC remain incompletely defined. - Source: PubMed
Publication date: 2026/07/27
Vokes Natalie ISymons Jessica LRhead BrookeHong LingzhiShah Pooja ALai ZhongwuZhu ZhouTreviño SantiagoBryan JulianWu JiaZhang JianjunGibbons DonHeymach John VStewart RossIyer SoniaLeventakos KonstantinosFragkogianni StamatinaChao CalvinRodon Jordi A - Ras GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) has been shown to bind cytosolic nucleic acid sensors including retinoic acid-inducible gene I (RIG-I) and cyclic GMP-AMP synthase (cGAS) in innate immunity. As a scaffolding protein enhancing protein-protein and protein-RNA interactions during cellular stress response, we examine whether G3BP1 could bind additional innate immune signaling molecules and investigate the relevance and mechanisms underlying these interactions. - Source: PubMed
Publication date: 2026/07/08
Song WenKim Susana Soo-YeonYam CandiceTeo JoeyLim Jyue YuanBi XuezhiLim Hong-HwaLam Kong-Peng - Protein arginine methyltransferases (PRMTs) catalyze arginine methylation, a key post-translational modification (PTM) regulating chromatin organization, RNA metabolism, and signaling. Recent studies reveal that PRMT-mediated methylation also modulates liquid-liquid phase separation (LLPS), which organizes membraneless condensates controlling transcription, stress response, and genome stability. Dysregulated PRMT activity disrupts condensate dynamics, contributing to cancer and neurodegenerative diseases. In cancer, PRMT1, PRMT5, and PRMT6 promote tumor progression via methylation-dependent condensates that enhance oncogenic transcription and stress resistance. In the nervous system, PRMT1, PRMT4, PRMT5, PRMT6, and PRMT8 regulate LLPS of proteins, linking aberrant methylation to ALS and Huntington's disease. This review highlights PRMTs as key modulators of phase separation and potential therapeutic targets in both oncology and neurodegeneration. - Source: PubMed
Publication date: 2026/07/22
Shen ZhihangYu Qiubin - Circulating cell-free epigenetic and epitranscriptomic modifications (epimarks) are emerging as minimally invasive biomarkers for cancer detection and therapeutic monitoring. Their clinical utility in non-small cell lung cancer (NSCLC), particularly in the context of EGFR-targeted therapies, remains to be fully established. Ten circulating epimarks encompassing cfRNA methylation, histone post-translational modifications on circulating nucleosomes, and cfDNA methylation were quantified in plasma samples from healthy donors and metastatic NSCLC patients with mutant or wild-type EGFR. Longitudinal analyses were performed in EGFR-mutant patients treated with tyrosine kinase inhibitors (TKIs). Functional relevance was assessed using in vitro and in ovo models of Osimertinib-sensitive and -resistant NSCLC cells combined with targeted epigenetic inhibitors. Distinct epimark signatures accurately discriminated healthy donors from NSCLC patients and distinguished EGFR-mutant from EGFR-wild-type tumors. cfRNA methylation marks (m1A, m6A, m5C, and m7G) showed excellent diagnostic performance, with a composite methyl-cfRNA score robustly distinguishing EGFR-mutant NSCLC. Disease progression under TKI therapy was characterized by increased m1A-cfRNA, H3K23Ac- and H4R3me2-circulating nucleosomes and decreased 5mC-cfDNA, with m1A-cfRNA alone reliably tracking progression. High m6A-cfRNA levels at diagnosis were strongly associated with shorter progression-free survival. Functionally, Osimertinib resistance promoted tumor growth and metastatic dissemination. Combination therapies targeting METTL3, KAT6A, or PRMT5 with Osimertinib reduced tumor burden and metastasis through miRNA-dependent regulation of histone acetylation and methylation. Circulating epimarks represent promosing diagnostic and prognostic biomarkers and provide a mechanistic basis for epigenetic combination therapies in EGFR-driven NSCLC. - Source: PubMed
Publication date: 2026/07/20
Espi-Bastien DorianRaimbourg JudithBougras-Cartron GwenolaNadaradjane ArulrajBlondeau SéverineDupas GuillaumeVolard BertrandLefrançois ArmelleGautier FabienMazières JulienMorin FranckMolinier OlivierBarlesi FabriceAmour ElodieDupé MathildeCartron Pierre-François - Defective endometrial decidualization is one major cause of female infertility, yet the underlying mechanisms remain elusive. Here, we identified that protein arginine methyltransferase 5 (PRMT5) which was upregulated during decidualization and by progesterone stimulation, is markedly down-regulated in the endometria of patients with recurrent implantation failure (RIF), along with a global reduction of symmetric dimethylarginine (sDMA). Uterine stromal-specific ablation of Prmt5 in mouse severely impaired decidualization leading to infertility. A multi‑omics analysis in human endometrial stromal cells (EnSCs) revealed that PRMT5 promoted decidualization primarily by catalyzing sDMA at arginine 346 (R346) of the orphan nuclear receptor Nur77, which directs its proper chromatin occupancy. Targeting the PRMT5-Nur77 methylation axis, we designed a peptide, Pep‑Nur77-R346K, which rescued the decidualization of multiple preclinical models: PRMT5 deficient human EnSCs, both genetic knockout (Prmt5d/d) and pharmacologically inhibited mouse models, an estrogen deficient mouse model, and, more importantly, the primary RIF EnSCs. In a retrospective cohort of 114 participants, the correlated reductions of endometrial PRMT5/Nur77-R346me2s was confirmed, which demonstrated robust predictive value for pregnancy outcome. Our work establishes the PRMT5‑Nur77 methylation axis as a key regulator of endometrial receptivity, and highlights both a novel diagnostic biomarker and a peptide‑based therapeutic potential for fertility. - Source: PubMed
Publication date: 2026/07/16
Cao ZhiwenCai XinyuMei JieKong NaLiu YangShen XiaoyueWu MinZhen XinSun JianxinLi RongJiang RuiweiSun HaixiangYan Guijun