Ask about this productRelated genes to: ICAM5 antibody
- Gene:
- ICAM5 NIH gene
- Name:
- intercellular adhesion molecule 5
- Previous symbol:
- TLCN
- Synonyms:
- TLN
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-15
- Date modifiied:
- 2015-11-13
Related products to: ICAM5 antibody
Related articles to: ICAM5 antibody
- DNA methylation influences gene-environment interactions and brain development in bipolar disorder (BD). We aimed to identify BD-associated epigenetic loci and examine their associations with brain structural variation. - Source: PubMed
Publication date: 2026/03/05
Yang Hyun-HoHan Kyu-ManKang YoubinShin DaunTae Woo-SukHan Mi-RyungHam Byung-Joo - Hypoglycemia is associated with cardiovascular events reflected by platelet abnormalities. We hypothesized that sequential endothelial changes may occur during hypoglycemia that may enhance cardiovascular risk. In type 2 diabetes (T2D) ( = 23) and controls ( = 23), blood SOMAscan proteomic analysis of endothelial proteins at baseline, insulin-induced hypoglycemia and post hypoglycemia to 24 h were examined using repeated-measures linear mixed modeling with a prospective parallel study design. Most endothelial proteins that changed over time did not differ between groups. Baseline levels of P-selectin, plasminogen activator inhibitor-1 (PAI-1; serpine-1), E-selectin and angiopoietin-1 (ANGPT1) were significantly higher, whilst cadherin-5 was lower in T2D. Several proteins exhibited changes versus baseline in both T2D and controls. Under hypoglycemia, decreases in cadherin-5 and soluble angiopoietin-1 receptor (sTie-2) were observed, with increased P-selectin, intercellular adhesion molecule-3 (ICAM3), ANGPT1 and PAI-1. Post hypoglycemia, decreased cadherin-5 and ICAM5 were observed at 2 h and PAI-1 at 4 h, as well as increases in P-selectin at 30 min, 1 h and 24 h and ICAM3 at 24 h. Post hypoglycemia, E-selectin, P-selectin and ICAM3 were significantly lower in T2D patients at 2 h, while PAI-1 was significantly lower at 4 h and ICAM3 was significantly lower at 24 h. Baseline endothelial proteins differed between T2D and controls, which may suggest local endothelial inflammatory activation leading to a pro-thrombotic, destabilized vascular phenotype characteristic of diabetic vasculopathy. Hypoglycemia may exacerbate this towards a pro-adhesive and pro-thrombotic phenotype, worsening endothelial dysfunction. - Source: PubMed
Publication date: 2026/01/14
Brennan EdwinaMoin Abu Saleh MdSathyapalan ThozhukatDempsey LauraAtkin Stephen LButler Alexandra E - Enterovirus D68 (EV-D68) is a globally reemerging respiratory pathogen of notable clinical concern due to its association with severe respiratory disease and the paralytic complication acute flaccid myelitis (AFM). Viral tropism and pathogenesis are critically dictated by interactions with host cell receptors. Our understanding of this process has evolved from a simple model of sialic acid dependence to a dynamic paradigm involving a repertoire of attachment factors and proteinaceous entry receptors. This review synthesizes the evolving landscape of EV-D68 receptor usage. We detail the well-established role of α2,6-linked sialic acid as an attachment factor and uncoating trigger for historical strains. We further discuss the discovery of intracellular adhesion molecule-5 (ICAM-5) as a neuron-specific receptor that provides a molecular explanation for neurotropism in AFM. A pivotal recent advance is the identification of major facilitator superfamily domain-containing 6 (MFSD6) as an essential entry receptor for a broad range of EV-D68 strains in both respiratory and neuronal cells. We explore the implications of this receptor versatility, whereby the virus can switch between or co-opt sialic acid, ICAM-5, and MFSD6, a plasticity that influences tissue tropism and viral evolution. Finally, we highlight how these mechanistic insights, particularly the characterization of the MFSD6 interface, are paving the way for novel therapeutic strategies, such as engineered decoy receptors, and outline key future directions in the field. - Source: PubMed
Publication date: 2025/12/30
Liu DongxueJi ZhilinZheng XiangyuXia HuimingYang WanshanGe Peng-FeiWei Wei - 5-Fluorouracil (5-Fu) is a cornerstone chemotherapeutic agent in the treatment of colorectal cancer (CRC). However, its clinical efficacy is frequently hampered by the development of drug resistance, which remains a major obstacle to successful treatment. The aim of this study is to gain a comprehensive understanding of the role and mechanism of the tumor cell-derived exosomal circ-0023919 in 5-Fu resistance. High-throughput microarray technology was employed to identify differentially expressed circRNAs in 5-Fu resistance CRC cells and their derived exosomes. A CRC/5-Fu drug-resistant cell line was successfully established using the drug gradient induction method, and its resistance index was subsequently determined. We employed transmission electron microscopy, nanoparticle tracking analysis (NTA) and Western blot to characterize exosomes by detecting the exosomal markers CD63 and TSG101. The circular structure, stability, and subcellular localization of circ-0023919 were confirmed using a combination of approaches, including actinomycin D treatment, RNase R digestion, specific primer PCR amplification, Sanger sequencing and FISH. Furthermore, we systematically evaluated the regulatory role of circ-0023919 in multiple biological functions of CRC cells by assessing cell proliferation, migration, invasion, drug resistance, stemness and EMT-related markers. Our findings demonstrate that circ-0023919 promotes the migration and invasion of CRC/5-Fu cells both in vitro and in vivo, while also enhancing resistance to 5-Fu chemotherapy. Mechanistically, circ-0023919 acts as a molecular sponge for miR-197-5p, thereby upregulating the expression of ICAM5. In this scientific study, circ-0023919 is shown to enhance the resistance of CRC cells to 5-Fu by promoting EMT. Thus, circ-0023919 is considered a potential therapeutic target for CRC treatment. - Source: PubMed
Publication date: 2025/12/13
Zhang JingjingWu YuanxiangWang YapingZeng Huihui - Current methods for isolating neuronal-derived extracellular vesicles (NDEVs) from human biofluids lack specificity. In addition, some of the reported markers for NDEV isolation are present as soluble proteins instead of extracellular vesicle (EV) associated proteins. To address the research gap, this study aimed to identify a novel marker for NDEV isolation that is NDEV associate and highly specific to the central nervous system. To achieve this, human cortical neurons were used for isolation of EVs . Mass spectroscopy was performed to screen for potential EV surface markers. This analysis yielded 63 brain specific proteins among which ICAM-5 was selected for further validations in human serum and cerebrospinal fluid (CSF) samples. Our analysis shows that ICAM-5 is present on the surface of NDEVs, colocalizing with standard extracellular vesicle markers like CD-63 and CD-9. We further confirm that NDEVs isolated using ICAM-5 contain neuronal proteins (tau, neuronal specific enolase) but not glial markers. Using ICAM-5 as a NDEV marker, EVs were eluted from human serum samples of with traumatic brain injury. Our results show enhanced levels of ubiquitin C-terminal hydrolase L1 (UCH-L1), a marker of neurological injury, in serum samples from patients with TBI when compared to currently known markers of NDEV. Our findings demonstrate that ICAM-5 is specific EV associated marker for isolating NDEVs from human biofluids that can potentially improve the enrichment of NDEVs from biofluids thereby improving diagnosis and monitoring of neurological conditions. - Source: PubMed
Publication date: 2025/11/10
Deleon PiperHattenberger ReaganKnollmann-Ritschel BarbaraBhomia Manish