PRMT5 Antibody
- Known as:
- PRMT5 Antibody
- Catalog number:
- 32297
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PRMT5 Antibody
Related genes to: PRMT5 Antibody
- 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
Related products to: PRMT5 Antibody
Related articles to: PRMT5 Antibody
- The epigenetic mechanisms driving the transition to ferroptosis in acute kidney injury (AKI) remain unclear. In this study, protein methyltransferase 5 (PRMT5) and its partner MEP50 were significantly upregulated in the renal tubules of AKI patients and murine models. Genetic silencing of PRMT5 via AAV-shRNA in vivo and siRNA in vitro improved renal function, attenuated mitochondrial damage, and suppressed ferroptotic tubular cell death. Mechanistically, PRMT5 promotes ACSL4 expression in a WDR5-dependent manner, facilitating tubular ferroptosis. Pharmacological inhibition of PRMT5 (GSK591) post-treatment or cloperastine hydrochloride prophylactic administration similarly improved renal function and limited ferroptotic cell death. These findings offer novel insights into the upstream epigenetic regulation of ACSL4-driven ferroptosis and suggest that PRMT5-ACSL4 axis might be a potential therapeutic target for AKI intervention. - Source: PubMed
Publication date: 2026/10/01
Lin JiawenFang JunxuanCui TianjiaoXu JiaqiLin WenjianLi ShupingSui YuanZheng ZhihuaWu KepingHuang Mingcheng - Biogenesis of UsnRNPs occurs in distinct steps in the nucleus and the cytoplasm. Sequential cytoplasmic actions of CLNS1A in the PRMT5 complex and of the SMN complex assemble the Sm core structure consisting of RNA and proteins. Nuclear SMN, condensed in Cajal Bodies, promotes late maturation steps. Whether cytoplasmic SMN undergoes condensation, and how this contributes to UsnRNP biogenesis or homeostasis, is poorly defined. Here, we show that molecular crowding stress induces rapid, reversible condensation of cytoplasmic SMN into droplets and filamentous assemblies, S-bodies, that sequester mislocalized cytoplasmic UsnRNPs along microtubules. During stress recovery, S-bodies undergo microtubule-dependent reorganization into split SMN-CLNS1A condensates, Janus bodies, that promote clearance of mislocalized UsnRNPs. Strikingly, cellular models of the SMN-associated disease spinal muscular atrophy fail to assemble S-bodies and to clear cytoplasmic UsnRNPs. Our findings identify stress-induced SMN condensation as a mechanism to buffer and resolve cytoplasmic UsnRNP mislocalization and reveal impaired tolerance to molecular crowding as a hallmark of spinal muscular atrophy. - Source: PubMed
Publication date: 2026/09/30
Riedel Yannick LDressler JessicaSchilling Maximilian TGruss Oliver J - Asthma is metabolically heterogeneous, but existing syntheses often place patient observations, animal perturbations, cross-disease mechanisms, and therapeutic concepts on the same evidentiary plane. This review addresses that problem by organizing glycolytic reprogramming and lysine lactylation through a three-tier hierarchy: human asthma observations, mechanistic perturbation in asthma-relevant models, and cross-disease or conceptual precedents. Mitochondrial and redox disturbances alter glycolytic and oxidative capacity across immune and structural cells, whereas lactate can function separately as an exported acidifying metabolite and as an intracellular substrate for site-specific lactylation. Four asthma-associated circuits have the strongest direct mechanistic support: epithelial histone H3 lysine 18 lactylation (H3K18la)-colony-stimulating factor 1 receptor (CSF1R) signaling; cluster of differentiation 4-positive (CD4) T-cell H3K18la-dipeptidyl peptidase 4 (DPP4) regulation; mitochondrial phosphoenolpyruvate carboxykinase 2 (PCK2)-dependent polyglutamine-binding protein 1 (PQBP1) K223 lactylation coupled to protein arginine methyltransferase 5 (PRMT5) inhibition; and macrophage sirtuin 6 (SIRT6)-lactate dehydrogenase A (LDHA)-histone H4 lysine 12 lactylation (H4K12la) signaling. Their prevalence, effect size, temporal stability, and distribution across human asthma phenotypes remain unknown, so they should not be considered validated endotypes or biomarkers. We therefore propose five mechanistically anchored research profiles and sequential analytical, biological, clinical, and external-replication gates, with falsification criteria and no universal numerical cutoffs absent empirical calibration. We further distinguish airway-restricted delivery from regional and cellular selectivity and define deposition, diseased-mucus transport, cell-resolved pharmacokinetics and pharmacodynamics, intracellular target engagement, and local-to-systemic safety as translational gates. The distinctive contribution is an evidence-graded, falsifiable framework that links metabolic state to cell- and residue-specific lactylation while making explicit what remains to be demonstrated in human asthma. - Source: PubMed
Publication date: 2026/09/15
Li ShuFang HaoxiangWang Kun - Acetyl tributyl citrate (ATBC) is an alternative plasticizer to Di(2-ethylhexyl) phthalate (DEHP) and bisphenol A (BPA) that may contribute to the development of various cancers. The cytotoxic activity and pro-tumorigenic role of ATBC in prostate cancer (PCa) progression remains poorly understood, highlighting the need for a systematic evaluation of its molecular toxicity. - Source: PubMed
Publication date: 2026/09/08
Xie ShangyanQing MingsongZhang ZihongZhang HangZhang YunxiaoYang ZhenyuChen ZhiweiLiang ZhuozhiA Garu - The therapeutic landscape of advanced melanoma has been transformed by immune checkpoint inhibitors and BRAF/MEK inhibitors, resulting in substantial improvements in response rates and overall survival. However, both primary and acquired resistance remain frequent, commonly driven by MAPK pathway reactivation and activation of compensatory signaling pathways. A persistent, unmet clinical need is particularly evident in certain molecular subgroups, including NRAS-mutant melanoma and tumors harboring non-V600 BRAF alterations. Better understanding of melanoma's molecular heterogeneity has led to the development of investigational targeted strategies beyond BRAF/MEK inhibition. These include next-generation MAPK pathway inhibitors, such as pan-RAF and ERK inhibitors, agents that target cell-cycle dysregulation, particularly in tumors with CDKN2A loss or CDK4/6 pathway activation. Epigenetic regulators, including PRMT5 inhibitors, are also being evaluated based on emerging preclinical evidence. Furthermore, alternative modalities such as targeted protein degradation platforms and antibody-drug conjugates directed against melanoma-associated antigens represent mechanistically distinct strategies. This review outlines the biological rationale for these approaches and summarizes available preclinical and early-phase clinical data. - Source: PubMed
Publication date: 2026/09/28
Dimitrakopoulou Marianna-ElisavetTheocharopoulos CharalamposKatsandri AikateriniFoteinou DimitraStefanou DimitraGkoufa AikateriniTsoukalas KonstantinosBousou ThaliaAnastasopoulou AmaliaGogas HelenZiogas Dimitrios C