Ask about this productRelated genes to: JAM3 antibody
- Gene:
- JAM3 NIH gene
- Name:
- junctional adhesion molecule 3
- Previous symbol:
- -
- Synonyms:
- JAM-C, JAMC
- Chromosome:
- 11q25
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-26
- Date modifiied:
- 2016-04-25
Related products to: JAM3 antibody
Related articles to: JAM3 antibody
- DNA methylation markers have been proposed as molecular triage tools for detecting cervical precancer and cancer, particularly among HPV-positive women. However, diagnostic performance varies across markers, assays, specimens, and clinical settings. This study aimed to evaluate the marker-specific diagnostic accuracy of DNA methylation markers and methylation panels for detecting CIN2+ and CIN3+ in cervical cancer screening, triage, and related diagnostic contexts. - Source: PubMed
Publication date: 2026/08/12
Horamee Sham Tahir AbdullaHosseini MostafaArabpour MaedehModarressi Mohammad Hossein - High-risk human papillomavirus (Hr-HPV) testing is highly sensitive for cervical cancer screening but lacks specificity, leading to unnecessary colposcopy referrals. Host-gene methylation and HPV viral load capture different aspects of disease risk and may support triage. - Source: PubMed
Publication date: 2026/08/27
Zhang YingChen ShuaiJiang YuZhang Lina - Primary brain calcification (PBC) is a neurodegenerative disorder characterized by bilateral brain calcification. JAM2 is a PBC causative gene, encoding the tight junction protein JAM2 and critical for blood-brain barrier (BBB) integrity, with an uncertain pathogenic mechanism. We analyzed two JAM2 missense mutations identified in PBC patients using plasmid constructs, immunoprecipitation, flow cytometry, and structural modeling. A Jam2 knockout (KO) mouse model was generated to assess behavioral deficits, brain calcification, and BBB integrity via histology, Evans blue assay, and in situ hybridization. JAM2-W108C mutants showed abnormal localization, while JAM2-R108H specifically disrupted JAM2-JAM3 interaction, mirroring the pathogenic JAM3-E116K mutation. Jam2 KO mice exhibited midbrain calcification (von Kossa staining) and motor impairments (rotarod/beam-walking tests) at 6-12 months. JAM2 and JAM3 co-localized in brain endothelial cells, and KO mice demonstrated BBB leakage (Evans blue extravasation). The main pathogenic mechanism of JAM2-PBC should be associated with the impaired JAM2-JAM3 heterodimer formation, compromising tight junctions and BBB integrity. Our study indicates JAM2-JAM3 interaction as a potential therapeutic target for PBC and related brain calcification disorders. - Source: PubMed
Publication date: 2026/08/27
Yang DehaoWang LeboYing ChenxinShi YihuaGuo YuruWang HaotianChen XinhuiWang YaotingWang XinchenZhang FanZheng XiaoshengChen YilingWang HaoyuLin ZhiruLi JiaxiangXia HaibinChen JiawenFu FengWang BoWu ShengWang PingXie FeiCen ZhidongWang ZhipingLuo Wei - Monocyte-endothelial interactions drive both acute inflammation and chronic vascular disease in type 2 diabetes mellitus (T2DM), yet whether TNF-α-induced and diabetes-associated monocyte trafficking engage similar or distinct molecular programs remains unclear. Using a physiological flow-based imaging system, we quantified CD14 monocyte adhesion, transendothelial migration (TEM), and abluminal residence on HUVEC monolayers activated with TNF-α or T2DM serum under controlled shear stress. Both stimuli induced comparable monocyte adhesion (~40 cells by 3 min), but TEM efficiency diverged markedly: TNF-α promoted robust TEM (~18% by 5 min) whereas T2DM conditions showed severely impaired TEM (~5%). Under T2DM conditions, monocytes exhibited prolonged abluminal retention (median 85 min vs. 25 min; p<0.0001), a phenotype recapitulated by endothelial hyperglycemic exposure alone. Comparative RNA-seq analysis of T2DM (GSE92724) and TNF-α-stimulated (GSE134489) endothelial cells revealed near-zero transcriptional correlation (r = 0.018) between conditions. TNF-α drove coordinate NF-κB-dependent upregulation of VCAM1, ICAM1, E-selectin, and junctional molecules with organized junctional remodeling, whereas T2DM produced VCAM1-biased adhesion with ICAM1 downregulation (0.61-fold), claudin suppression, and junctional disorganization. KEGG pathway mapping confirmed organized endothelial-leukocyte integrin co-activation under TNF-α versus discoordination junctional loss under T2DM. qPCR validation identified selective RAGE and JAM3 upregulation under T2DM-consistent with AGE-RAGE signaling and JAM-3-MAC-1 monocyte trapping-without classical NF-κB activation. These findings define two fundamentally distinct paradigms: a TNF-α "recruitment model" enabling efficient trafficking and resolution, versus a T2DM "retention model" characterized by VCAM1-biased adhesion, junctional disorganization, and impaired reverse transmigration driving chronic monocyte accumulation, identifying AGE-RAGE signaling and JAM-3-MAC-1 interactions as potential therapeutic targets for diabetic vascular inflammation. - Source: PubMed
Publication date: 2026/07/10
Semo DilvinLiang XiaoheSchwietzer MarielWang WeiqiHu XiaokangDorenkamp MarcPoorana Priya PrabhakaranManogaran Joshua MartinVincent Franklin ChristopherReinecke HolgerGodfrey Rinesh - This prospective study aimed to evaluate the efficacy of 5-aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) for cervical/vaginal intraepithelial neoplasia (CIN/VaIN) and explore the predictive value of pretreatment PAX1/JAM3 methylation status in exfoliated cells for treatment outcomes. - Source: PubMed
Publication date: 2026/06/25
Han QinWu ZhangxinGuo Hongyan