Ask about this productRelated genes to: PLAGL1 Blocking Peptide
- Gene:
- PLAGL1 NIH gene
- Name:
- PLAG1 like zinc finger 1
- Previous symbol:
- -
- Synonyms:
- ZAC, LOT1
- Chromosome:
- 6q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-17
- Date modifiied:
- 2019-04-23
Related products to: PLAGL1 Blocking Peptide
Related articles to: PLAGL1 Blocking Peptide
- Source: PubMed
- Central nervous system embryonal tumour with PLAGL amplification, a methylation-defined tumour entity, may lack typical embryonal morphology. In this paediatric case, the diagnosis was established by DNA methylation profiling and confirmed by fluorescence in situ hybridisation demonstrating PLAGL1 amplification. Recognition of this morphology-molecular discordance may help avoid diagnostic pitfalls. - Source: PubMed
Okuse RyoNobusawa SumihitoKurose AkiraKamataki AkihisaSato YuichiSugimoto RyoSuzuki HiromichiYanagawa NaokiBeppu Takaaki - Transcription factor (TF) networks are pivotal regulators of stem/progenitor cell fate. However, the regulatory mechanisms mediated by key TFs in adult periosteal stem/progenitor cells (PSPCs) remain poorly understood, impeding targeted therapies development for craniofacial bone regeneration. By integrating an analysis of regeneration-related, tissue-specific TF networks with insights from embryonic development, we demonstrate that the imprinted TF PLAGL1 is critical for the osteoblast differentiation of PSPCs and that the loss of Plagl1 compromises mandibular bone regeneration. Mechanistically, PLAGL1 transcriptionally activates TF Irx5 synergistically with TF KLF4, thereby inducing the expression of downstream osteogenic genes. Using the CRISPR-dCas9-Tet1-CD/sgRNA system, we develop a differentially methylated region-targeted therapeutic strategy to reactivate the maternal allele of Plagl1, leveraging its imprinted function to promote mandibular bone regeneration. This study delineates the PLAGL1-KLF4-IRX5 regulatory axis controlling osteoblast differentiation of PSPCs and further proposes an application strategy integrating TF modulation with epigenetic regulation for craniofacial bone regeneration. - Source: PubMed
Publication date: 2026/05/21
Yao EnhuiLiu YiliXu JingyiXu ZeqianHuang YileiZhou MingliangLin SihanJiang XinquanDu Jiahui - Periodontitis leads to alveolar bone resorption, driven by persistent periodontal pathogen infection. Such persistent infection creates a unique microenvironment conducive to sustained reactive oxygen species (ROS) production. Therefore, further investigation into approaches that simultaneously combat bacteria and improve the local microenvironment is needed. In the present study, a hydrogel drug delivery system was proposed, which employed an in-situ synthesis strategy of zeolitic imidazole frameworks 90 (ZIF90) encapsulating tungsten (W)-based polyoxometalate nanoparticles (ZIF90-W) to increase the W ratio and confer ATP responsiveness. ZIF90-W was incorporated into phenylboronic acid-modified quaternary ammonium salt chitosan hydrogel (QPT hydrogel), forming QPT@ZIF90-W hydrogel with responsive release properties in the periodontal pocket. Results demonstrated that QPT@ZIF90-W hydrogel exhibited over 90% antibacterial efficacy against periodontal pathogens. Besides, QPT@ZIF90-W significantly promoted osteogenic differentiation of MC3T3-E1 cells after scavenging mitochondrial ROS and total ROS. Mechanistically, the pro-osteogenic effect of QPT@ZIF90-W hydrogel was associated with the significant upregulation of Plagl1, following oxidative stress elimination and subsequent activating the Wnt signaling pathway, according to the transcriptome sequencing results. Concurrently, in vivo experiments demonstrated that QPT@ZIF90-W hydrogel treatment, compared with other groups, reduced inflammatory cell infiltration, upregulated Plagl1 and osteogenesis related proteins, and partially ameliorated alveolar bone resorption. In summary, QPT@ZIF90-W is characterized by synergistic antibacterial effect and ROS scavenging capability. These dual activities reshape the oxidative microenvironment and then activate Plagl1/Wnt pathway to promote osteogenesis, which offer a novel and potential strategy for the precise treatment of periodontitis-induced bone defects. - Source: PubMed
Publication date: 2026/05/14
Yu ZhenyuanLi YuchaoZhang ShuweiCao RuoyanLiu KunDeng JiaqiYang ZeWang HongyanWang QiangMiao LeiHu BoPan Yaping - MicroRNAs direct downregulation of target mRNAs. Sometimes, however, this regulatory paradigm inverts, and a target RNA triggers degradation of a microRNA. This target-directed microRNA degradation (TDMD) requires ZSWIM8. mice exhibit reduced growth and perinatal lethality, accompanied by stabilization of >40 microRNAs. Nonetheless, studies of TDMD function in mammals have been limited because only two TDMD-triggering RNAs have been identified in mice. Here, we computationally identify and validate five new TDMD-triggering sites in mouse models. One site in and two sites in direct degradation of miR-335-3p, showing that in mammals, two sites in the same transcript and multiple sites in different transcripts can collaborate to destabilize a microRNA. Moreover, sites in and direct degradation of miR-322 and miR-503, respectively. Mice lacking the and sites were smaller, demonstrating that target-directed degradation of miR-322 and miR-503 promotes growth. Both miR-335-3p and are maternally imprinted, implying their participation in parental conflict, but their corresponding triggers or target microRNA partners are not imprinted. Thus, 3' UTRs can participate in parental conflict not only by regulating protein production but also by engaging TDMD to access an additional layer of regulation within a network of imprinted and biallelic genes. - Source: PubMed
Publication date: 2026/04/01
Lin Daniel HElcavage Lara EKhalizeva EkaterinaBartel David P