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
- 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 - Cervical intraepithelial neoplasia grade 3 (CIN 3)-like squamous cell carcinoma (SCC) is a recently identified subtype of cervical cancer with a deceptive growth pattern. It mimics the phenotype of CIN 3, involving endocervical crypts, presenting significant challenges and potential for diagnostic confusion. This study aims to clarify the differences in epigenetic profiles and HPV viral load(VL) among CIN 3, CIN 3-like SCC, early invasive SCC, and invasive SCC. - Source: PubMed
Publication date: 2026/07/10
Li MingzhuZhang XiaoboZhao XingWang JixianZhao ChaoZhao YunLi JingranShen DanhuaWei Lihui - To investigate the risk factors associated with pathological progression of cervical lesions, specifically focusing on high-risk human papillomavirus (HR-HPV) infection, ThinPrep Cytologic Test (TCT), and PAX1/JAM3 gene methylation in a high-risk colposcopy-referred cohort. - Source: PubMed
Publication date: 2026/06/25
Geng TongyaoLi SijiaBian YananLi XiaodongBian Yahui - [This retracts the article DOI: 10.1155/2022/6423237.]. - Source: PubMed
Publication date: 2026/06/11
Markers Disease