Ask about this productRelated genes to: PRMT2 antibody
- Gene:
- PRMT2 NIH gene
- Name:
- protein arginine methyltransferase 2
- Previous symbol:
- HRMT1L1
- Synonyms:
- MGC111373
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2017-12-15
Related products to: PRMT2 antibody
Related articles to: PRMT2 antibody
- Spinal cord injury (SCI) is a devastating disorder of the central nervous system (CNS) leading to irreversible neurological deficits. Effective pharmacotherapy remains elusive, due to the restrictive blood-spinal cord barrier (BSCB), underscoring the urgent need for targeted and efficient drug delivery strategies. Luteolin (LUT), a natural flavonoid with potent anti-neuroinflammatory properties, presents a promising therapeutic option; however, it is compromised by poor solubility, low bioavailability, and limited BSCB penetration. Drawing inspiration from the traditional Chinese medicine concept of the "orifice-opening" effect of borneol (BO), we developed BO-modified mesoporous silica nanoparticles (MSN-BO@LUT) for targeted LUT delivery to the spinal cord. MSN-BO@LUT significantly enhanced LUT delivery to the spinal cord, achieving a 286.36-fold increase over LUT, and maintained a concentration of 802.17 ng/mL at 24 h. MSN-BO@LUT demonstrated robust anti-neuroinflammatory and neuroprotective effects in SCI mice, reducing microglial infiltration, promoting functional recovery, and showing favorable efficacy and safety compared with the positive control methylprednisolone. Mechanistically, released LUT targets protein arginine N-methyltransferase, reduces toll-like receptor 4 methylation, and inhibits nuclear factor kappa B-mediated pro-inflammatory signaling, thereby suppressing microglial M1 polarization. These findings suggest that MSN-BO@LUT not only provides a developed, safe, effective nanotherapeutic strategy for SCI treatment but also serves as a translatable template for developing precision nanomedicines targeting CNS disorders. - Source: PubMed
Publication date: 2026/09/27
Wang YixuanJin BoLi ShipianOuyang QianxiXiao YuWen JiaxinLai YehuaWang PingWang YongjunCui XuejunZhang WeianYao Min - Endothelial-to-mesenchymal transition (EndMT) is implicated in cardiac remodeling under pathological stress, although its full in vivo occurrence may be context-dependent. Emerging evidence suggests that protein methylation is an important post-translational modification involved in regulating endothelial phenotypic transition (EndMT-like process). However, the role of protein arginine methyltransferase 2 (PRMT2), a key protein arginine methyltransferase, in modulating endothelial phenotypic transition-particularly in the context of cardiac remodeling-remains poorly understood. - Source: PubMed
Publication date: 2026/08/03
Fan XianweiLi XuejieHu JuanYan LijieWu JintaoZhang LeimingLiu JingjingYang Haitao - Intervertebral disc degeneration (IVDD) is a leading cause of low back pain, yet there remains no effective therapeutic approach to reverse its progression, imposing a substantial socioeconomic burden. While multiple factors contribute to IVDD pathogenesis, cellular senescence has emerged as a critical risk factor associated with both the incidence and progression of IVDD. Aging and other damage factors drive nucleus pulposus cells (NPCs) toward a senescent phenotype characterized by increased secretion of proinflammatory factors, resulting in NPC dysfunction and tissue degeneration, which are hallmarks of IVDD. In this study, we demonstrated that PRMT2 deficiency disrupted arginine methylation-ubiquitination crosstalk, driving NPC inflammatory senescence and accelerating IVDD progression. Mechanistically, PRMT2 loss reduced FBXO7 methylation at Arg504, promoting the FBXO7-MED12 interaction to facilitate MED12 ubiquitination and subsequent proteasomal degradation. MED12 deficiency induced pathological R-loop accumulation, which activated the cytosolic DNA-sensing cGAS/STING axis, triggering inflammatory response cascades. Notably, engineered extracellular vesicles delivering MED12-overexpressing plasmids significantly inhibited NPC senescence and attenuated IVDD progression. Together, our findings establish that dysregulated methylation-ubiquitination crosstalk critically drives IVDD progression and reveal MED12 as a promising therapeutic target for ameliorating the impact of IVDD. - Source: PubMed
Publication date: 2026/06/30
Liang HuaizhenZhu DingchaoDu ZhiLi XinyuShi RuiLei JieTong BideXu HanpengWu DiZhou XingyuDu YifanOu ZixuanWei JunyuPeng ShuchangKe WencanLiao ZhiweiWang BingjinWang KunFeng XiaoboSong YuYang Cao - Down syndrome (DS) features impaired cortical neurogenesis and excess gliogenesis, yet the temporal regulatory events driving this imbalance remain unclear. Here, we combine multi-timepoint transcriptomic analyses from publicly available datasets, network modelling, and machine-learning prioritization, with validation in isogenic human iPSC-derived cerebral organoids, to identify a discrete pathogenic window at 90 days in vitro (DIV 90). Across five developmental stages, REST target genes were preferentially dysregulated in DS organoids. WGCNA revealed a DS-associated module at DIV-90 that strongly overlapped with REST targets, and two orthogonal machine-learning approaches converged on six REST-regulated hub genes-CSTB, MCM3AP, PFKL, POFUT2, PRMT2, and RWDD2B. In trisomic organoids, REST mRNA and nuclear protein were markedly reduced at DIV-90, accompanied by diminished DCX expression and activation of NFIA and STAT3, suggesting a neurogenic-to-gliogenic fate transition. These findings suggest REST dysfunction as a potential temporal regulator of lineage imbalance in DS and highlight REST-linked networks as potential targets for early developmental intervention. - Source: PubMed
Publication date: 2026/05/16
Huang TanLim Chong-TeikLi WeiFakurazi SharidaMason John OCheah Pike-SeeLi YiLing King-Hwa - Microglia serve as the principal instigators of neuroinflammatory cascades following ischemic stroke. We here demonstrated that PRMT2IP (previously named as 1700017B05Rik in mice and C15orf39 in humans) is essential for modulating microglial activation and functional responses in ischemic stroke. Mendelian randomization (MR) analysis demonstrated a causal relationship between downregulation of human PRMT2IP expression and an elevated risk of ischemic stroke. Mouse PRMT2IP expression was downregulated in ischemic microglia. Critically, PRMT2IP overexpression provided a protective role in reducing cerebral ischemia injury, while PRMT2IP knockout showed significantly worsened outcomes. Mechanistically, PRMT2IP interacts with PRMT2 and inhibits the activation of the NF-κB signaling pathway by PRMT2-IκBα signaling axis, ultimately reducing the expression of inflammatory factors IL-6 and TNFα. In conclusion, our results suggest that microglial PRMT2IP, as a key negative regulator of microglial inflammatory response, alleviates ischemia-induced brain injury. Thus, up-regulation of PRMT2IP expression may provide a therapeutic strategy to attenuate deleterious neuroinflammation post-stroke. - Source: PubMed
Publication date: 2026/03/24
Zhang MinCai JiexunSu WentingZeng QiZhang HuaweiDeng JiahuiZhai BingXiao HeZhu GaizhiGao RanQiu JinmingBian ZiqingLuan GuomingWang Renxi