CD106 (human) _ Clone 1299_27_1
- Known as:
- CD106 (H. sapiens) _ Clone 1299_27_1
- Catalog number:
- T-1126.0200
- Product Quantity:
- 200ìg
- Category:
- -
- Supplier:
- New Immunology
- Gene target:
- CD106 (human) _ Clone 1299_27_1
Related genes to: CD106 (human) _ Clone 1299_27_1
- 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 (human) _ Clone 1299_27_1
Related articles to: CD106 (human) _ Clone 1299_27_1
- Activation of innate immunity early after reperfused myocardial infarction (MI) contributes to reperfusion injury and acts systemically to accelerate atherosclerosis in remote non-culprit plaques. We hypothesized that inhibition of the NLRP3 inflammasome complex that is activated by damage-associated molecular patterns after MI would suppress these diverse maladaptive responses. - Source: PubMed
Publication date: 2026/07/16
Karnewar SantoshNguyen The AnhOzawa KoyaHuang WeitingVarli OnurMorello MatteoLindner Emma LCasarez Eli VXie ArisLópez José AKelly JazminToldo StefanoAbbate AntonioLindner Jonathan R - Acute respiratory distress syndrome (ARDS) remains a critical condition associated with high morbidity and mortality, particularly when triggered by sepsis. Endothelial dysfunction is a central hallmark of ARDS pathology, but the precise mechanisms underlying pulmonary microvascular dysfunction remain poorly understood. Extracellular vesicles (EVs) have emerged as crucial mediators of cell-cell communication during inflammation; however, their role in endothelial dysfunction in ARDS is less clearly defined. We utilized a human pulmonary microvascular endothelial cell (HPMEC)-based model of sepsis-induced acute lung injury to investigate whether inflammatory EVs (iEVs), derived from endothelial cells treated with bacterial lipopolysaccharide (LPS), impair naïve HPMEC function. EVs were characterized by nanoparticle tracking analysis, transmission electron microscopy, and immunofluorescence, confirming purity and uptake. iEV exposure significantly reduced barrier integrity by electric cell-substrate impedance sensing (ECIS) and increased cell migration; effects partially reversed by the TLR4 inhibitor TAK-242. Adhesion and tube formation were unaffected. Pre-treatment of donor HPMECs with the neutral sphingomyelinase inhibitor GW4869 attenuated the barrier-disrupting capacity of the resulting iEVs, implicating ceramide-dependent EV biogenesis in generating pathogenic cargo. Trypan Blue staining confirmed that these effects reflect altered signaling rather than cell death. iEV exposure upregulated TLR4, MyD88, IL-6, ICAM-1, VCAM-1, E-selectin, and Jag1 mRNA, with TAK-242 attenuating IL-6 and ICAM-1 induction. Our results highlight endothelial-derived EVs and TLR4-dependent pathways as amplifiers of pulmonary vascular injury in sepsis-induced ARDS, identifying EV biogenesis and EV-mediated signaling as novel therapeutic targets. - Source: PubMed
Publication date: 2026/07/17
Cohen MayaHaigis LianaBlum RebeccaSherman-Roe AllysonPereira MandyChichger HavoviVentetuolo Corey ELiang OlinHarrington Elizabeth O - This study was aimed at systematically characterizing cell-type-specific cholesterol metabolism in human blood samples, and investigating the impact of hypercholesterolemia on the composition and gene expression of immune and stromal populations. Single-cell RNA sequencing (scRNA-seq) data from 31 human blood samples, encompassing 472,204 high-quality circulating cells, were analyzed. Pathway activities were assessed via gene set variation analysis (GSVA), and cell-type-specific markers were identified using differential expression analysis. Clinical cholesterol levels were used to stratify samples for comparative analysis of cell abundance and transcriptional changes. Monocytes and macrophages were found to exhibit heightened activity in cholesterol transport and dynamic response pathways. Five monocyte-enriched cholesterol metabolism genes (CSF3R, FPR1, MNDA, MPEG1, and VCAN) were identified. Hypercholesterolemia was associated with increased abundance of macrophages, T cells, and NK cells, as well as decreased B cells and monocytes. Significant upregulation of pro-inflammatory genes such as VCAM1 in high-cholesterol conditions was revealed by differential gene expression analysis. Our study provided a comprehensive cell-type-specific atlas of cholesterol metabolism in human blood cells, highlighting metabolic heterogeneity and hypercholesterolemia-induced immune remodeling in the circulation. This resource offered novel insights into cholesterol-mediated immunomodulation. - Source: PubMed
Publication date: 2026/07/17
Chu JianZhuang JingHan ShuwenLiang YujiuMao JingZhang ZianChu CaiyunYang Xi - Age is the most important risk factor for coronary artery disease (CAD) independent of traditional risk factors. Aging induces classic pro-inflammatory and prothrombotic vascular phenotypic changes whose molecular mediators remain poorly understood. Medin is a common cleavage product protein that accumulates in vasculature with aging and shown to cause endothelial dysfunction. Its role in CAD is unknown. The study aimed to evaluate the effects of medin on human coronary artery endothelial cell (HCAEC) pro-inflammatory and prothrombotic activation and establish the relationship between medin and coronary atherosclerosis in human decedents. - Source: PubMed
Publication date: 2026/07/07
Morrow KalebKaramanova NinaWoltjer RandyKrajbich VictoriaShu JingminLi MingTang ChengyunMaerivoet AlanaMadine JillianChen YabingMigrino Raymond Q - Spatial profiling of proteins and protein interactions facilitates understanding of cell functions within tissues and is essential for studies in signaling, immunity, and cancer. We present spatial proximity sequencing (Sprox-seq) for simultaneous profiling of surface proteins, protein complexes, and mRNAs, recording the tissue location of each molecule. Sprox-seq profiled 32 proteins, 528 pairwise interactions, and thousands of mRNAs with spatial resolution across human tonsils and germinal centers. Mapping tissue-wide protein interactions recapitulated RNA-defined tissue architecture but also revealed higher interaction complexity in the light zone. Protein-interaction trajectories uncovered a B cell state transition distinct from that inferred by RNA. Integrated protein-complex and mRNA analysis related spatially enriched complexes with mitotic pathways. Sprox-seq captured cell-cell interactions, such as B cell-follicular dendritic cell interactions mediated by the receptor complex VLA-4-VCAM1. Sprox-seq provides a spatially resolved multi-modal view of cell states and an integrated study of protein and cellular interactions across tissues. - Source: PubMed
Publication date: 2026/07/16
Wang HuiliXia JunjieRahman Peer Mohamed Suhail MujiburKeisham BijentimalaPadhi AbinashDeng YiyuLi YanVistain LukeKim SarahMercado-Vásquez GabrielKhan Aly AClark Marcus RTay Savaş