Ask about this productRelated genes to: PARD3 Blocking Peptide
- Gene:
- PARD3 NIH gene
- Name:
- par-3 family cell polarity regulator
- Previous symbol:
- -
- Synonyms:
- PAR3, PARD3A, Bazooka, Baz, ASIP, PPP1R118
- Chromosome:
- 10p11.22-p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-27
- Date modifiied:
- 2018-02-13
Related products to: PARD3 Blocking Peptide
Related articles to: PARD3 Blocking Peptide
- Periodontitis (PD) is a chronic inflammatory disease characterized by dysregulated immune responses and periodontal tissue destruction. While T lymphocytes are implicated in PD pathogenesis, the roles of specific T cell subsets remain unclear. - Source: PubMed
Publication date: 2026/08/24
Ren FukaiLiu XiqianYan Bin - Ameloblastin (Ambn) is a tooth-specific multifunctional protein essential for enamel biomineralization and the formation of its prismatic microstructure. To examine the function of the evolutionarily conserved cell-binding Ambn amphipathic helix (AH) motif, we deleted the hydrophobic residues within the Ambn AH motif in genetically engineered mice. Enamel in the homozygous (Ambn) mutants had normal thickness but was hypo-mineralized and lacked prismatic structure. Micro-CT analysis further revealed that both the secretory and maturation stages of amelogenesis were delayed and proceeded slower than in the controls. Ameloblasts in the mutants were stunted and exhibited loss of cell polarity, as demonstrated by the mislocalization of Pard3, Claudin-1 and GM130 immunosignals. In the Ambn mutants, a loss of Ambn-ameloblast distal membrane interaction was observed, with nuclear localization of β-catenin and p-Smad2/3, and a decrease in RhoA immunolabeling intensity, suggesting that changes in known signaling pathways may connect Ambn-cell interactions to the establishment of cell polarity. Together, these findings support a model in which AH-dependent Ambn engagement at the distal ameloblast membrane contributes to secretory-stage polarity and prism patterning, with downstream consequences for enamel organization and maturation-stage mineral density. - Source: PubMed
Publication date: 2026/08/20
Visakan GayathriBapat Rucha ArunCai JingSuwandi Ethan TrevorJoester DerkKegulian Natalie CSarkisians EdwinAghazadeh MarziyehWebster SimonMoradian-Oldak Janet - Endometrial injury-related disorders, including intrauterine adhesions, thin endometrium, and chronic endometritis, are a major cause of female infertility. Conventional therapeutic approaches, primarily hormone therapy and surgical interventions, show limited effectiveness in patients with moderate to severe endometrial damage. In this context, regenerative medicine has emerged as a promising direction to overcome current therapeutic limitations and promote functional reconstruction of the endometrium. A comprehensive literature search was conducted across PubMed, Web of Science, Embase, and Scopus to identify relevant studies on endometrial repair and regenerative medicine. The search covered publications from January 2000 to August 2025. The following keyword combinations and MeSH terms were used: ("endometrial repair" OR "endometrial regeneration" OR "intrauterine adhesion" OR "Asherman syndrome" OR "thin endometrium" OR "chronic endometritis") AND ("mesenchymal stem cells" OR "platelet-rich plasma" OR "exosomes" OR "extracellular vesicles" OR "biomaterials" OR "hydrogel" OR "scaffold" OR "regenerative medicine"). Both basic science investigations and clinical studies were included to provide a comprehensive overview of current developments in the field. To minimize the risk of omission, the reference lists of included articles and relevant reviews were manually screened, and potentially pertinent studies were further evaluated. Inclusion criteria: (1) Original research articles or meta-analyses; (2) Focus on therapeutic interventions for endometrial regeneration; (3) Human clinical studies or mammalian animal models. Exclusion criteria: (1) Non-English articles, letters, conference proceedings, etc.; (2) Purely descriptive studies of endometrial physiology without therapeutic intervention, articles lacking quantitative data or sufficient methodological details. The screening process followed the PRISMA 2020 guidelines (Fig. 1). After removing duplicates, 1936 records were screened by title and abstract, and 605 full-text articles were assessed for eligibility. Finally, 102 studies were included in this qualitative synthesis. This review provides a systematic synthesis of recent advances in cell-based therapies, cell-free approaches, and bioengineering strategies for endometrial repair. Evidence derived from different sources of mesenchymal stem cells, including bone marrow, umbilical cord, and endometrium, is comparatively evaluated alongside platelet-rich plasma and extracellular vesicles, with an emphasis on hierarchical assessment of evidence levels. Several critical issues are further examined. Current stem cell-based interventions are largely characterized by a broad reparative profile, yet precise targeting of key molecular mechanisms remains insufficient. To date, no studies have demonstrated the capacity to directly reverse suppression of signaling pathways such as the GZMA-PARD3 axis or to restore depleted regenerative stromal subpopulations, including IGFBP3⁺ cells. Clinical investigations of platelet-rich plasma exhibit substantial heterogeneity, which appears to stem mainly from the absence of standardized preparation protocols and the frequent reliance on surrogate endpoints, particularly endometrial thickness. However, the predictive value of endometrial thickness for live birth is limited, and its use as a primary endpoint may overestimate clinical benefit. Therefore, emphasis should shift toward patient-centered outcomes such as live birth rate. Concerns also arise regarding the degradation kinetics of biomaterials, as mismatches between material resorption and the cyclical regenerative dynamics of the endometrium may increase the risk of secondary adhesions. In addition, the actual delivery efficiency of microneedle-based systems within the enclosed and humid uterine environment has not yet been fully clarified. Based on this critical appraisal, we propose a translational framework that links mechanistic discovery with precision intervention. The importance of long-term follow-up is emphasized, with live birth rate regarded as a more clinically meaningful primary endpoint for evaluating therapeutic efficacy in endometrial regenerative medicine. Endometrial regenerative medicine is transitioning from empirical repair toward mechanism-informed reconstruction. Current evidence is dominated by short-term (< 12 months), small-sample (n < 50) exploratory studies with high interventional heterogeneity. Clinical translation will require unified preparation standards, individualized treatment strategies, and well-designed multicenter randomized controlled trials with live birth rate as the primary endpoint and minimum 2-year follow-up. - Source: PubMed
Publication date: 2026/07/27
Xie MengqiCao YunguiTang JiangpingLi FangDeng Juan - Long non-coding RNAs (lncRNAs) play crucial roles in the onset and progression of cardiovascular disease, particularly atherosclerosis. However, the role of PARD3-AS1 in atherosclerosis remains largely uncharacterized. This study therefore aimed to investigate the impact of the PARD3-AS1/miR-668-3p axis on atherosclerosis. The expression levels of PARD3-AS1 and miR-668-3p in human umbilical vein endothelial cells (HUVECs) were quantified by quantitative real-time polymerase chain reaction (RT-qPCR). HUVEC proliferation was assessed using a Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) incorporation, and migratory and invasive capacities were evaluated using wound healing and Transwell assays. The interaction between PARD3-AS1 and miR-668-3p was confirmed by bioinformatics analysis and dual-luciferase reporter assays. In addition, serum samples were collected from patients diagnosed with atherosclerosis, and ApoE⁻/⁻ C57BL/6 mice were fed a high-fat diet for 8 weeks to establish a model of atherosclerosis. PARD3-AS1 expression was significantly reduced in the serum of patients with atherosclerosis, whereas miR-668-3p levels were markedly elevated, and the two were negatively correlated. Subsequent experiments confirmed that miR-668-3p effectively reversed the promotion effects of PARD3-AS1 on HUVEC proliferation and migration. In vivo, histological staining showed that the PARD3-AS1 overexpression group exhibited improved endothelial repair. Collectively, these findings demonstrate that PARD3-AS1 directly interacts with miR-668-3p to modulate HUVEC proliferation, migration, and invasion, suggesting that PARD3-AS1 may serve as a potential therapeutic target for atherosclerosis. - Source: PubMed
Publication date: 2026/07/21
Sun XiaozhiZhang LinlinWang XinxingYan JunweiJiao XuefeiLi YongxinGuo Mingjin - To identify and validate differential mRNA N-methyladenosine (mA) methylation sites associated with mild cognitive impairment (MCI), providing potential molecular evidence for its early prevention and intervention. A case-control study was conducted among older adults recruited from multiple community health centers in Shenzhen, including a pilot cohort (5 pairs) and a validation cohort (25 pairs). Single-based mA quantitative polymerase chain reaction was used to quantify plasma mRNA mA methylation levels. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed, followed by the construction of a protein-protein interaction network to identify hub genes. The differential methylation levels of key genes were validated in an expanded cohort. For normally distributed data, -tests were used; for non-normal data, Mann-Whitney or tests were applied. Partial correlation analysis and Firth logistic regression were conducted to verify the associations further. A total of 126 differential mRNA mA methylation sites were identified, including 73 upregulated and 53 downregulated sites. Five hub genes (, , , , and ) were selected, based on protein-protein interaction network topology. Validation experiments showed that the mRNA mA methylation levels of these five genes were significantly higher in the MCI group than in healthy controls (all <0.001). After adjustment for potential confounders, partial correlation analysis revealed that the methylation levels of all five genes were negatively correlated with MMSE scores (=-0.719- -0.426, all <0.05). Firth logistic regression confirmed that these genes were independently associated with MCI (=1.57-2.88, all <0.001). This study screened and verified a range of MCI-related differential mA methylation sites, suggesting that abnormal mA methylation of specific gene mRNAs may be associated with MCI, providing research clues for further exploration of the molecular mechanism of MCI and potential plasma molecular markers. - Source: PubMed
Yan HWang X LWei S THuang Q MGao JChen P LZhang Y XZhong W FYang JChen HXie J HLiu DLi Z HMao C