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
- 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 - Trisomy 21 (T21) is the genetic cause of Down syndrome (DS), and the presence of extra genetic material causes altered expression of genes located on chromosome 21 (Hsa21) and others, with effects as altered levels of metabolic reaction products. The one‑carbon pathway plays a central role in correct human neurodevelopment and was found to be altered in DS and neurological impairments of different entities. In this work, the expression of 42 genes involved in the one‑carbon cycle was analyzed in blood samples from 10 subjects with T21 and 10 euploid (N) subjects. Additionally, plasmatic concentration of methylcobalamin (MeCbl) was evaluated in 10 subjects with T21 and 7 N subjects. The results showed that 13 genes out of 42 were differentially expressed: 11 were over-expressed (ABCC3, ABCC4, ARMT1, CTH, FOLR2, GART, ICMT, PRMT2, SETD4, SLC19A1, and NSD2) and 2 were under-expressed (NSUN3 and TRMT112). Among these, 4 over-expressed genes are located on Hsa21 (GART, PRMT2, SETD4, and SLC19A1). Statistical analyses revealed significant correlations between gene expression data, highlighting interconnections among genes. Finally, MeCbl shows a slight statistically significant reduction in the T21 group. In conclusion, the presence of three copies of Hsa21 leads to the dysregulation of gene expression associated with the one‑carbon cycle. This dysregulation affects genes located on both Hsa21 and other chromosomes resulting in metabolic alterations. Additionally, new gene interconnections were discovered that have not been previously reported in the literature. - Source: PubMed
Publication date: 2025/11/27
Vione BeatriceGaudesi Alessandro MariaAntonaros FrancescaCicilloni MichelaVitale LorenzaPiovesan AllisonPelleri Maria ChiaraStrippoli PierluigiSperti GiacomoRamacieri GiuseppeCatapano FrancescaParadisi PietroPirazzoli Gian LucaCorvaglia Luigi TommasoLocatelli ChiaraCaracausi Maria - Histone arginine methylation by protein arginine methyltransferases (PRMTs) is crucial for transcriptional regulation and is implicated in cancers. Despite their therapeutic potential, some PRMTs present challenges as drug targets due to their context-dependent activities. Here, we demonstrate that hypoxia triggers the rapid condensation of PRMT2, which is essential for its histone H3R8 asymmetric dimethylation (H3R8me2a) activity. This process depends on PRMT2's integration into transcriptional condensates, which is mediated by phosphorylation at Serine 12 within its N-terminal intrinsically disordered region. This phosphorylation is critical for hypoxia-inducible gene expression and glioblastoma (GBM) progression. Transcription-associated cyclin-dependent kinases (CDKs), particularly CDK9, drive PRMT2S12 phosphorylation. Inhibition of CDK9 using TG02 suppresses hypoxia-induced H3R8me2a and transcriptional activity. Moreover, the combination of TG02 and temozolomide, the standard chemotherapy for GBM, significantly inhibits tumor progression in mouse xenograft models, an effect partially mediated by targeting PRMT2S12 phosphorylation. Our study uncovers the role of transcriptional condensation in enhancing PRMT activity, reveals a new mechanism for CDK9 inhibitors in modulating context-dependent transcriptional programs, and proposed a combinatorial therapeutic strategy against GBM. - Source: PubMed
Publication date: 2025/09/05
Dong FengCheng XuanWan JiaxiangLi QianDu WeijianLi WeiSun XiaoyuWu Xudong - Protein arginine methyltransferases (PRMTs) are a class of enzymes that mediate critical post-translational modifications through arginine methylation as epigenetic regulators. PRMTs have been shown to have a vast array of regulatory effects including in gene expression, signal transduction, and cellular proliferation. Dysregulation of PRMT activity has been seen in the progression of various cancers, including breast, lung, and colorectal cancer. Moreover, PRMT overexpression has been shown to correlate with poor patient prognosis. This review aims to explore the roles of the individual PRMTs in cancer and aims to highlight the latest and newest developments of PRMT inhibitors as emerging therapeutic strategies. Numerous preclinical and clinical studies have identified several novel compounds that effectively target PRMT activity and have shown significant therapeutic results. As such, this review aims to not only highlight the current research findings, but to also emphasize the significant need for future research on PRMTs as novel therapeutic targets in cancer. - Source: PubMed
Publication date: 2025/08/16
Kaganovski AdrianaSmith-Salzberg BayleShimshon Hadar KDraheim AndrewSpivak MarkSapir TzurielShifteh David - Protein arginine methyltransferase 2 (PRMT2) is a critical epigenetic modulator that orchestrates diverse biological processes through histone methylation-dependent transcriptional regulation. While previous studies have established its pro-inflammatory role in murine colitis, the oncogenic functions and immunomodulatory mechanisms of PRMT2 in colorectal cancer (CRC) pathogenesis remain elusive. In this study, integrated analysis of TCGA database, colorectal cancer single-cell database, and CRC patient-derived tissue microarrays revealed significant upregulation of PRMT2 in tumor tissues, which correlated with adverse clinical outcomes and reduced survival rates. Mechanistically, we found that PRMT2 can promote the transcriptional expression of WNT5A, thereby activating the Wnt/β-catenin signaling pathway and malignant progression of CRC. Notably, our study uncovered the dual immunoregulatory role of PRMT2 in shaping the tumor microenvironment. PRMT2 not only induced M2-like polarization of tumor-associated macrophages (TAMs) but also impaired anti-tumor T cell responses by promoting CD4/CD8 T cell dysfunction. In conclusion, our findings position PRMT2 as a multifaceted therapeutic target that simultaneously addresses tumor intrinsic malignancy and microenvironmental immunosuppression in CRC. - Source: PubMed
Publication date: 2025/08/09
Zou HailinLiu YangruiyuYang XiaotingZhang QingyuanPan QingmingHuang JiaxinGuo YaoyuZhou YijunFang ShuoChen Zhe-ShengPan Yihang