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
- Glycyrrhizic acid (GL), a natural triterpenoid glycoside extracted from the "medicine food homology" herb L., exhibits potent anti-atherosclerotic effects; yet its underlying mechanisms remain unclear due to its poor oral bioavailability. The gut microbiota plays a pivotal role in the development of atherosclerosis (AS). In this study, the microbiota-dependent anti-AS effects of GL were evaluated in high-fat diet (HFD)-fed mice using antibiotic depletion and fecal microbiota transplantation (FMT). Integrated metagenomic and metabolomic analyses were performed to identify the key bioactive microbial metabolite. Further in vivo and in vitro experiments, including co-immunoprecipitation and dual-luciferase reporter assays, were utilized to elucidate the underlying molecular mechanisms. It was demonstrated that oral administration of GL alleviated AS in a microbiota-dependent manner by reversing gut dysbiosis, improving intestinal barrier function, and reducing pro-inflammatory lipopolysaccharide (LPS) levels. GL shifted intestinal tryptophan metabolism toward bacterial-derived indole-3-lactic acid (ILA) production, suppressing LPS-induced vascular endothelial adhesion dysfunction by activating the aryl hydrocarbon receptor (AhR). Mechanistically, ILA-activated AhR interacted with the NF-κB subunit p65 in the cytoplasm, effectively preventing the nuclear translocation of p65 and suppressing the promoter activities of adhesion molecules ( and ), resulting in the amelioration of HFD-induced AS. These findings elucidate the microbiota-dependent mechanism of orally administered GL against AS, and highlight the therapeutic potential of targeting the ILA-AhR-p65 axis in the vascular endothelium as a strategy for AS. - Source: PubMed
Publication date: 2026/07/27
Shen HaoranHuang ShuaiWang ZhiyuZhou SitongHuang LuluZhang HongjuanHan YanxingJiang JiandongGuo Huihui - 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