Ask about this productRelated genes to: CD106 antibody
- Gene:
- VCAM1 NIH gene
- Name:
- vascular cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- CD106
- Chromosome:
- 1p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2016-10-05
Related products to: CD106 antibody
Related articles to: CD106 antibody
- Internal N7-methylguanosine (mG) is a recently identified chemical modification of mammalian mRNA. Although the epitranscriptome plays a key role in regulating RNA metabolism and cellular function, the specific contribution of internal mG to cardiovascular disease remains unknown. Atherosclerosis preferentially develops at sites of disturbed blood flow, which promotes endothelial activation; however, whether internal mG regulates endothelial mechanotransduction and atherogenesis remains unclear. - Source: PubMed
Publication date: 2026/08/11
Shentu Tzu-PinWu TongZhou ZhengjieLi JinYeh Chih-FanZhu JiayuHuang Ru-TingMiao Bernadette AXi BrianLo JasonCarver LaurynLee Tzu-HanZhang LishengHarrison DevinHodonsky Chani JAuguste GaelleArasu Uma ThanigaiKaikkonen-Määttä MinnaHusain Aliya NTirrell Matthew VMiller Clint LDickinson Bryan CYang Kai-ChienFang Yun - To investigate the protective effect of lipocalin-2 (LCN2) gene knockout against sepsis-induced acute lung injury (ALI) and vascular endothelial dysfunction in mice and the mediating role of the nuclear factor-κB (NF-κB) signaling pathway. - Source: PubMed
Yu MengjieZhao AnboHao YixuanWang YirenLiu YuexianYe HongweiGao Qin - Integrin α4β7 is a key adhesion receptor that mediates lymphocyte homing to the intestinal mucosa through interactions with MAdCAM-1, VCAM-1, and fibronectin, thereby playing a central role in gut immune surveillance and mucosal immunity. Emerging evidence has expanded its functional scope beyond intestinal homeostasis to encompass diverse inflammatory and metabolic diseases. This review systematically summarizes the structural characteristics, ligand interactions, and conformational regulation of α4β7, with an emphasis on its pathogenic roles in inflammatory bowel disease, cardiovascular diseases, diabetes, liver disorders, autoimmune diseases, gastrointestinal malignancies, HIV infection, asthma, and graft-versus-host disease. We discuss the underlying mechanisms, including lymphocyte trafficking, T cell co-stimulation, immune subset dysregulation, and crosstalk with the gut microbiota and epithelial barrier. In addition, we review the current landscape of α4β7-targeting therapeutics, including vedolizumab, etrolizumab, ontamalimab, and small-molecule antagonists, highlighting their clinical applications and limitations. By integrating recent mechanistic insights and therapeutic advances, this review provides a comprehensive framework for understanding the multifaceted roles of α4β7 and informs future strategies for targeting this integrin in disease. - Source: PubMed
Publication date: 2026/08/05
Chen YueChen YongZhang ZhiyuanTao MengxingGeng Chi - Blood-brain barrier (BBB) integrity naturally declines with age. Brain endothelial cells (ECs) and pericytes (PCs) form the BBB, and aging impairs tight junctions, likely via altered PC-to-EC signaling. However, the molecular mechanisms underlying this impairment remain unclear. Using single-cell RNA sequencing, we profiled 68,316 brain ECs expressing 15,564 genes from young and old mice. Unsupervised clustering and annotation revealed five distinct EC subtypes-Capillary EC1, Capillary EC2, Arterial EC, Venous EC1, and Venous EC2-defined by marker genes , and , respectively. Aging shifted EC subtype distribution, with reduced Capillary EC1 (45% vs. 57%) and increased Arterial (33% vs. 16%) and Venous ECs (12% vs. 2%) compared with young mice. Mio analysis further showed that Capillary EC1 and Venous EC2 neighborhoods were less abundant in aged brains. Biotin metabolism was decreased in old vs. young mice, particularly within Capillary EC1, Capillary EC2, and Arterial EC. Although widespread gene downregulation was observed across EC subsets, overall expression trends were largely consistent among clusters. Key genes--were less abundant, whereas was uniquely enriched in aged mice. Immunohistochemistry confirmed reduced LY6C and RAMP2 and elevated RASGRF2 in aged mouse and human brains. Cell-cell interaction analyses revealed age-associated remodeling of ligand-receptor signaling. Enrichment analyses implicated pathways involved in neurovascular integrity, inflammation, amyloid processing, and vascular remodeling. Collectively, these findings show that aging reprograms EC subtype composition, gene expression, and metabolism, thereby contributing to BBB disruption and neurovascular dysfunction. - Source: PubMed
Publication date: 2026/07/31
Nguyen Hai DucSiddiqui SummerBohannon Diana GBlair Robert VDeng Hong-WenPrat AlexandreKim Woong-Ki - Globally, acute ischemic stroke (AIS) continues to be a major contributor to death and long-term functional impairment. The present work investigates the clinical relevance of miR-369-3p in AIS and how it regulates brain microvascular endothelial cells. Quantitative measurements of serum miR-369-3p were conducted in a cohort comprising 138 individuals with AIS and 120 healthy controls. ROC curve analysis and Cox proportional hazards regression were employed to evaluate diagnostic and prognostic performance of miR-369-3p. Human brain microvascular endothelial cells (hCMEC/D3) were exposed to oxygen-glucose deprivation followed by reoxygenation (OGD/R), allowing assessment of how miR-369-3p influences cell viability, inflammatory responses, and the expression of adhesion molecules. Downstream target genes were identified through bioinformatics analysis and validated using a dual-luciferase assay. A statistically significant reduction in serum miR-369-3p levels was observed among AIS patients relative to controls (P < 0.001), and this miRNA demonstrated favorable diagnostic accuracy. Lower expression of miR-369-3p emerged as an independent predictor of poorer functional outcomes, as assessed by the modified Rankin Scale (mRS) score at 90 days post‑stroke. In cellular studies, upregulation of miR-369-3p mitigated the loss of cell viability induced by OGD/R, reduced the production of pro‑inflammatory cytokines and lowered the levels of ICAM‑1 and VCAM‑1. Furthermore, VAV3 was confirmed as a direct target of miR-369-3p; restoring VAV3 expression counteracted the protective effects conferred by miR-369-3p. Serum miR-369-3p may serve as a non-invasive diagnostic and prognostic biomarker for AIS. Mechanistically, miR-369-3p protects against ischemic endothelial injury by targeting VAV3 and mitigating inflammation and adhesion molecule expression. - Source: PubMed
Publication date: 2026/08/08
Zhang MeijieYin LidaLiu ZhixinMeng YanruLi YueMeng JinhuiYin Xueyong