PTDSR Blocking Peptide
- Known as:
- PTDSR Blocking Peptide
- Catalog number:
- 33r-7320
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PTDSR Blocking Peptide
Ask about this productRelated genes to: PTDSR Blocking Peptide
- Gene:
- JMJD6 NIH gene
- Name:
- jumonji domain containing 6, arginine demethylase and lysine hydroxylase
- Previous symbol:
- PTDSR
- Synonyms:
- PTDSR1, KIAA0585
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-09
- Date modifiied:
- 2018-07-12
Related products to: PTDSR Blocking Peptide
Related articles to: PTDSR Blocking Peptide
- Jumonji domain-containing protein 6 (JMJD6) has been implicated in epigenetic regulation. Here, we demonstrated that JMJD6 was upregulated during pseudorabies virus (PRV) infection and critically enhanced viral replication by promoting virion release. Mechanistically, JMJD6 suppressed PRV-induced histone H4K16 acetylation, a modification associated with chromatin relaxation and DNA damage response activation. This epigenetic modulation attenuated the cGAS-STING-mediated innate immune signaling pathway, leading to reduced interferon production and enhanced viral propagation. Furthermore, we identified METTL23 as a nuclear interactor of JMJD6 upon viral infection, revealing a cooperative role between these proteins in facilitating immune evasion. Importantly, administration of the JMJD6-specific inhibitor JMJD6-IN-1 potently activated innate immunity and restricted PRV replication in mice. Our findings unveil a novel epigenetic strategy employed by PRV to evade host antiviral responses and highlight JMJD6 as a potential therapeutic target for combating herpesvirus infections.IMPORTANCEThe ongoing conflict between viruses and host antiviral defenses is central to viral pathogenesis. Pseudorabies virus (PRV), a highly contagious alphaherpesvirus, causes severe economic losses in the global swine industry and poses an emerging zoonotic threat to humans. This study identifies the epigenetic modulator, the JMJD6, as a critical host factor exploited by PRV to evade antiviral immunity. Our work uncovers a previously unrecognized epigenetic strategy employed by herpesviruses and establishes JMJD6 as a promising target for developing broad-spectrum antivirals against PRV and related pathogenic herpesviruses. - Source: PubMed
Publication date: 2026/04/29
Ming Sheng-LiChai Ya-JingYang Jia-MingXing Jia-YouZhang Shi-JunHe Sai-NanLu Qing-XiaWang JiangPan Jia-JiaLu Wei-FeiZeng LeiChu Bei-Bei - Drought stress is a major abiotic factor limiting maize yield and stability. Although Jumonji C (JMJ) histone demethylases are known to regulate plant growth, development, and stress responses, their systematic characterization in maize has remained limited. Here, 27 genes were identified in the maize genome through BLAST and conserved-domain analyses and classified into five subfamilies: JMJD6, KDM3/JHDM2, KDM4/JHDM3, KDM5/JARID1, and JmjC domain-only. Members within the same subfamily showed similar physicochemical properties, domain composition, and motif distribution, whereas clear divergence was observed among subfamilies. Chromosomal mapping revealed that genes were unevenly distributed across nine chromosomes, with two interchromosomal homologous gene pairs, suggesting roles for segmental and/or whole-genome duplication in family expansion. Promoter analysis indicated widespread enrichment of elements related to light responsiveness, growth and development, and hormone and stress responses. Expression profiling showed that most genes were highly expressed in leaves, while several displayed tissue specificity. Under drought stress, , , , and were significantly induced, highlighting them as promising candidates for functional studies and molecular breeding for drought tolerance in maize. This study provides a foundation for elucidating the evolution and functions of the family and identifies candidate genes for drought-related functional validation and molecular breeding. - Source: PubMed
Publication date: 2026/03/27
Gao LiTian HuiBai XiangliShi AokunWang Mian - JMJD6, a bifunctional epigenetic modulator within the Jumonji C family, has garnered increasing attention for its potential roles in tumorigenesis, yet its pan-cancer prognostic and mechanistic significance remain incompletely characterized. In this study, we performed a comprehensive pan-cancer analysis of JMJD6 using multi-omics data from public databases including TCGA, CPTAC, HPA, and GEPIA2. Our results revealed that JMJD6 is significantly overexpressed across cancers and positively correlated with advanced tumor stage and unfavorable patient survival outcomes. Mechanistically, JMJD6 overexpression was associated with promoter hypomethylation and showed close interactions with RNA modification regulators. Furthermore, JMJD6 expression correlated significantly with immune cell infiltration, elevated genomic instability (TMB, MSI, HRD), and differential sensitivity to targeted therapies such as EGFR inhibitors. Functional enrichment analysis underscored its involvement in spliceosome and chromatin remodeling pathways. Collectively, our findings establish JMJD6 as an influential oncogene and robust prognostic biomarker across cancer types, with implications for future therapeutic strategies targeting epigenetic and immune pathways. - Source: PubMed
Publication date: 2026/03/18
Liu LihuaLi TaoHe JingLiu Guiling - Cancer stem cells are involved in chemotherapy resistance. Neuroblastoma (NB) is a common solid tumor in children, which is responsible for about 15% of pediatric cancer deaths. Jumonji domain-containing 6 (JMJD6), which is an arginine demethylase and lysine hydroxylase, regulates the progression of various tumors. However, the molecular mechanism underlying JMJD6's activity in NB stem cells remains unclear. Thus, this study aims to explore the role of JMJD6 in NB stem cells. - Source: PubMed
Publication date: 2026/01/14
Li ZuoqingGao WenzongGao PengfeiFei YingchunChen HuadongJiang HongXie JuntaoXu Zhe - The therapeutic efficacy of extracellular vesicles (EVs) depends on the status of their donor cells. Cellular senescence of bone marrow mesenchymal stem cells (BMSCs), which induces significant changes to cellular secretome, greatly affects the osteogenesis of the donor BMSCs along with BMSC-derived EVs. Stem cells prefer a homeostatic self-renewing state to alleviate the senescence and loss of stemness caused by external disturbance, but which inevitable in EV produce. In this study, to avoid the senescence of BMSCs caused by in vitro culture and boost the osteogenesis efficacy of BMSC-derived small extracellular vesicles (sEVs), we established a niche-mimicking (NM) culturing system to maintain the cellular homeostasis that significantly delayed stem cell senescence in vitro. As a result, single cell transcriptome revealed that NM-culturing significantly enhanced the expression level of the homeostasis-related genes. Then we found that sEVs produced by homeostatic BMSCs exhibited superior osteogenic stimulation efficacy and bone defect repair compared to those from conventional monolayer-cultured BMSCs. Mechanically, by analyzing the "shuttling effect" of sEVs via multi-omic analysis, we found that the key homeostasis-related genes (including JMJD6, LIF, CYP19A1, and LAMA1) functioned throughout the entire process, by thus we defined the "homeostatic phenotype" of BMSC. Among the identified homeostasis-related genes in sEVs, JMJD6 emerges as a key gene, exhibiting anti-senescence characteristics and stimulating osteogenesis via Wnt pathway in BMSCs. This study optimizes the production part of stem cell-based EV therapy by maintaining the cellular homeostasis of donor cells, which delays cell senescence and boosts the osteogenesis stimulation of EVs, and JMJD6 is a key homeostasis-related gene that regulated cell senescence and osteogenesis of BMSC. - Source: PubMed
Publication date: 2026/02/21
Fu SongningLiu LuXu FengCheng JinLiu YadongLiu TianyuFu ChangfengWu YanhuaZhou NanYang QiweiWang Yuanyi