CD106 (VCAM) Adhesion Molecule Antibody
- Known as:
- CD106 (VCAM) Adhesion Molecule Antibody
- Catalog number:
- MAB357C
- Product Quantity:
- 0.5 ml
- Category:
- -
- Supplier:
- INNOVEX
- Gene target:
- CD106 (VCAM) Adhesion Molecule Antibody
Related genes to: CD106 (VCAM) Adhesion Molecule 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 (VCAM) Adhesion Molecule Antibody
Related articles to: CD106 (VCAM) Adhesion Molecule Antibody
- Long noncoding RNAs (lncRNAs) are key regulators of vascular endothelial function. The lncRNA differentiation antagonizing non-protein coding RNA (DANCR) is implicated in cell proliferation and inflammatory responses; however, its specific role in atherosclerosis remains undefined. - Source: PubMed
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Wang ShutingZhang QiyueLi RongxiaWang YixiaoKamili AdalaitiHan YuqingHou ZhihuiChen YuYang ShujunZhang Weili - Zaoshi Huatan Xiefei Formula (ZHXF) is a Chinese medicine prescription used in the treatment of severe pneumonia (SP). Although clinical studies have confirmed its efficacy in improving pneumonia, the specific bioactive components and their intricate regulatory pathwaysremain incompletely understood. - Source: PubMed
Publication date: 2026/08/22
Shan BaixiZhao ShuaijunZhang ZhijingCao HaiyangJiang YuhangDu YanZhang QinZhao PengLi Jiansheng - Aging is a progressive, multisystem process characterized by declining physiological resilience and increased susceptibility to chronic diseases. Recent advances in high-throughput proteomics have enabled comprehensive mapping of age-related changes across circulating proteins, revealing dynamic and non-linear trajectories that reflect biological rather than chronological aging. This review synthesizes current evidence on proteomic biomarkers across major physiological systems, including the immune, metabolic/endocrine, cardiovascular, musculoskeletal, and nervous systems, and highlights shared molecular signatures that underpin multisystem decline. Robust biomarkers such as IL-6, CRP, CXCL9/10, GDF15, IGF-1, VCAM-1, NT-proBNP, NfL, and GFAP consistently track inflammatory activation, mitochondrial and metabolic stress, extracellular matrix remodeling, and neuro-glial injury. Large population cohorts demonstrate that proteomic aging clocks, leveraging dozens to hundreds of circulating proteins, can predict frailty, multimorbidity, organ-specific biological age, and mortality with high accuracy. Emerging evidence suggests that a limited set of cross-system "protein aging modules"-including inflammatory cytokines, chemokines, complement proteins, and ECM-modifying enzymes-may serve as integrative readouts and potential regulators of aging biology. We discuss methodological advances, system-specific mechanisms, and translational applications of proteomic aging models. Together, these findings position proteomics as a powerful tool for quantifying biological age, identifying early disease risk, and guiding precision interventions to promote healthier aging. - Source: PubMed
Publication date: 2026/08/14
Luo YingXiao Yu-LinChen Jie-HuaWang HongjueLuo ShuhongDong HuaHuang Ruo-Pan - Aging is a major risk factor for cardiovascular diseases (CVD), partly due to the accumulation of senescent cells. Senescence is characterized by irreversible cell cycle arrest and the acquisition of a senescence associated secretory phenotype (SASP), which promotes inflammation and tissue remodeling, thereby contributing to cardiac dysfunction. Cardiac fibroblasts (CFs), key regulators of cardiac repair, differentiate into myofibroblasts (CMFs) in response to pathological stimuli such as mechanical stiffness and TGF-β1. CMFs secrete abundant extracellular matrix (ECM) proteins, and while their senescence may transiently restrict fibrosis in acute cardiac injury, persistent senescence promotes chronic remodeling through SASP activity. Given that TGF-β1 is a central mediator of CF-to-CMF differentiation and can induce senescence in various cell lines, we investigated whether it simultaneously triggers both processes in neonatal rat CFs, and whether the senotherapeutics Navitoclax and Dasatinib + Quercetin modulate the viability of senescent CMFs. - Source: PubMed
Publication date: 2026/08/14
Espinoza-Perez ClaudioOsorio José MiguelVélez RubénOrtega Bustos JuanMachuca VíctorRivas SebastiánSánchez-Ferrer Carlos FPeiró ConcepciónVivar RaúlDíaz-Araya Guillermo - Aging is accompanied by an increasing prevalence of frailty and age-related cognitive decline (CD). Cognitive frailty (CF), characterized by physical frailty and cognitive impairment, has been associated with oxidative stress, neuroinflammation, mitochondrial dysfunction, and cardiovascular impairment. However, its biological foundations remain only partially understood. This review synthesizes evidence on biomarkers associated with the blood-brain barrier (BBB) and neurovascular unit (NVU) in CD and CF. These biomarkers are associated with endothelial injury, pericyte damage, BBB permeability, tight junction disruption, glial activation, and extracellular vesicles (EVs). They are assessed by analyzing cerebrospinal fluid (CSF), blood, neuroimaging (including DCE-MRI), and histology. The most frequently evaluated markers were CSF sPDGFRβ, the CSF/serum albumin ratio (QAlb), DCE-MRI permeability, and the adhesion molecules ICAM-1 and VCAM-1. Key convergent findings suggest that BBB breakdown (particularly pericyte injury, as indicated by elevated CSF sPDGFRβ) can precede or occur independently of classical amyloid-β and tau pathology, predict CD in APOE4 carriers over up to 4.5 years, and be associated with disrupted default mode network connectivity. Elevated QAlb demonstrated dose-response prognostic value for clinical deterioration, while DCE-MRI permeability was associated with poorer episodic memory and predicted white-matter injury, which mediated cognitive impairment. Endothelial activation markers were elevated early and predicted progression, whereas vWF exhibited a stage-dependent, potentially biphasic association. Overall, BBB/NVU biomarkers support vascular and neuroinflammatory mechanisms as early, partially Alzheimer's disease-independent contributors to CD and CF, with significant modification by APOE4 and metabolic comorbidities, and with distinct signatures across Alzheimer's disease and vascular cognitive impairment. - Source: PubMed
Publication date: 2026/08/28
Rodríguez-Callejas Juan de DiosMimenza-Alvarado Alberto JoséLomas-Soria ConsueloAguilar-Navarro Sara Gloria