Mouse ICAM-1 ELISA Kit
- Known as:
- Mouse ICAM-1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 21730
- Product Quantity:
- 96T
- Category:
- Peptides
- Supplier:
- Bio-Medical
- Gene target:
- Mouse ICAM-1 ELISA Kit
Related genes to: Mouse ICAM-1 ELISA Kit
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
Related products to: Mouse ICAM-1 ELISA Kit
Related articles to: Mouse ICAM-1 ELISA Kit
- Intron retention, a form of alternative RNA splicing, can occur as part of normal gene regulation or result from disruption of the splicing machinery. Retained introns can potentially form double-stranded RNA, activating innate immune sensors and inflammation. This mechanism has been implicated in cancer but has not been studied in neuropsychiatric diseases like alcohol use disorder. We systematically analysed transcriptome-wide intron retention events in brain tissue from 142 individuals (66 with alcohol use disorder and 76 controls), encompassing 320 region-specific samples from the superior frontal cortex, nucleus accumbens, central nucleus and basolateral amygdala. Analyses were adjusted for demographic, technical and biological covariates. Validation was performed in alcohol-preferring (P) rats using long-read sequencing. In complementary experiments, immunofluorescent staining was used to detect double-stranded RNA in rat brain tissue, while single-cell RNA-sequencing was performed to test activation of double-stranded RNA-sensing pathways in human brains. Brains from individuals with alcohol use disorder showed significantly higher total intron retention compared with controls, independent of age, with females showing greater increases than males. A total of 368 introns were positively associated with alcohol use disorder, and these introns were significantly longer and had weaker splice acceptor sites compared with non-associated introns. Genes harbouring these intron retention events were enriched in Purkinje neurons, visual cortex neurons and oligodendrocytes. Computational predictions indicated these long introns could form duplex RNA structures. Increased double-stranded RNA was confirmed experimentally in multiple brain regions of alcohol-consuming rats, where it co-localized primarily with neuronal nuclei and dendrites. In individuals with alcohol use disorder, we found that multiple pathways including double-stranded RNA responses, neuroinflammation, interferon and NF-κB signalling, adaptive immunity and apoptosis were activated. In addition, NeuN-positive neuronal counts significantly decreased in both the prefrontal and visual cortices. Furthermore, single-cell analysis demonstrated upregulation of TICAM1, the target of double-stranded RNA sensor TLR3, in oligodendrocytes, as well as widespread activation of downstream inflammatory pathways across glial and neuronal cell types. These findings provide the first evidence that chronic alcohol consumption promotes an overall increase of intron retention in the brain and is associated with the presence of double-stranded RNA. Furthermore, the double-stranded RNA may contribute to neuronal loss and brain pathology by activating a neuroinflammatory response. - Source: PubMed
Publication date: 2026/07/29
Li RudongReiter Jill LWyatt-Johnson Season KDong ChuanpengSmith Caine SGreen NickGao HongyuHauser Sheketha RKapoor ManavStevens JuliaMayfield R DayneGoate AlisonWang YueEdenberg Howard JBell Richard LSutherland Greg TrevorBrutkiewicz RandyLiu Yunlong - This study aimed to investigate the relationship between the molecular weight of carboxymethyl pachymaran (CMP) and its immunomodulatory activities, and to identify the molecular weight range responsible for activating the TLR4 pathways. Thirteen kinds of CMPs with different molecular weights ranging from 49 kDa to 655 kDa were obtained using enzymatic degradation. The structure of CMPs was characterized by FT-IR, NMR, XRD, TGA, and SEM. We found that the reduction in molecular weight modified the surface morphology of CMP, while the main structure remained unchanged. Our results indicated that CMP0 (655 kDa) failed to exert immunomodulatory effects by activating the TLR4/MyD88/NF-κB and TLR4/TRIF/IRF3 pathway. The CMPD12 (112 kDa) activated both TLR4/MyD88/NF-κB and TLR4/TRIF/IRF3 signaling pathways, promoted the secretion of NO, TNF-α, IL-6, IL-1β, and IFN-β in RAW264.7 cells, and induced M1 polarization, thereby exerting the optimal immunomodulatory activity. In contrast, CMPD60 (49 kDa) failed to activate the TLR4/MyD88/NF-κB pathway to induce the secrete of NO and cytokines in RAW264.7 cells, it only activated the TLR4/TRIF/IRF3 pathway to promote IFN-β secretion and M1 polarization in macrophages, exerting weak immunomodulatory activity. Our results revealed the molecular weight range responsible for the immunomodulatory activities of CMP, suggesting its potential application as an immunomodulating agent. - Source: PubMed
Publication date: 2026/07/18
Zhang LijiaHuang WenFeng XiMei ZhinanLiu Ying - High pathogenicity avian influenza (HPAI) poses a significant threat to poultry. Some chickens show resilience to HPAI, but the mechanisms involved are poorly understood. In this study, we aimed to identify the biological mechanisms associated with resilience to HPAIV infection in chickens. Chickens were inoculated with H7N1 HPAIV and classified as susceptible or resilient based on clinical signs, mortality, histopathological lesions, AIV antigen detection in tissues, and viral shedding. Blood transcriptomic analysis revealed that genes from resilient chickens are involved in the integrin-mediated signaling pathway (ITGA5, ITGA6, ITGB1), as well as in adaptive (BTK, TEC) and innate (TRIM13, LCK, TICAM1) immune pathways. Plasma proteomic profiling revealed that ARF4, EIF4A2, and HNRNPAB (proteins involved in fundamental cellular processes) were less abundant in resilient chickens compared to both controls and susceptible birds. Our results suggest that early modulation of these pathways is associated with resilience to HPAIV and likely reflects early viral control or reduced systemic dissemination rather than the absence of infection. - Source: PubMed
Publication date: 2026/08/06
Valdez-May María JPerlas AlbertNofrarías MiquelPina-Pedrero SoniaDabad MarcValle RosaPérez MartaMoreno-León AlejandroEsteve-Codina AnnaArgilaguet JordiBertran KateriMajó Natàlia - The ubiquitin ligase protein tripartite-motif containing 56 (TRIM56) positively regulates Toll-like receptor-3 (TLR3) signaling by forming a complex with Toll-Interleukin-1 receptor domain-containing adapter protein inducing interferon (IFN)-beta (TRIF), independent of its E3 ligase activity. Whether TRIM56 modulates other TLR pathways in innate antiviral immunity, however, is unclear. Herein, we show ectopic expression of TRIM56 augments activation of IFN regulatory factor-3 (IRF3)-dependent promoters following stimulation by lipopolysaccharide (LPS) in HEK293-TLR4-MD2-CD14 cells while leaving activation of NF-κB-dependent promoter unaffected, suggesting TRIM56 specifically promotes immune signaling through the TLR4-TRIF axis but not the MYD88 arm downstream of this TLR. Confirming its impact on endogenous antiviral responses in immune sentinel cells naturally harboring the TLR4 pathway, we demonstrated enforced expression of TRIM56 enhanced LPS-induced expression of IFN-beta and IFN-stimulated genes (ISGs) and establishment of an antiviral state in bone marrow-derived macrophages. Importantly, depletion of endogenous TRIM56 impaired LPS-induced antiviral gene expression and cellular antiviral defense. Altogether, these data add to understanding of the role of TRIM56 in TLR-mediated innate immune responses. Given that TRIM56 is an ISG and that many immune adjuvants and some viral proteins activate TLR4, the findings of this study could have implications for designing immunotherapies, especially those against viral infections. - Source: PubMed
Publication date: 2026/07/19
Tong XiaohanLi Nan LYang DarongLiu Benjamin MLi Zhuoyuan AlexLi Kui - Central nervous system (CNS) inflammation triggered by viral infections plays a crucial role in the pathogenesis of various neurological diseases. Microglia, as the resident immune cells of the CNS, detect viral components via Toll-like receptors (TLRs) and activate downstream inflammatory signaling pathways, such as NF-κB and mitogen-activated protein kinase (MAPK), which trigger a cascade of pro-inflammatory cytokines. Excessive immune responses often lead to neuronal damage and neurodegeneration. Phenethyl isothiocyanate (PEITC) is a small molecule derived from plants; previous studies have indicated its potential to modulate TLR-related signaling pathways and to exert immunomodulatory effects. This study investigates whether PEITC can inhibit Poly (I:C)-induced microglial inflammatory responses and related signal transduction pathways. Thus, we first conducted cell experiments using BV2 mouse microglial cells. The results showed that Poly (I:C) stimulation significantly upregulated NO and various pro-inflammatory factors (e.g., TNF-α, IL-1β, IL-6). At the same time, PEITC pre-treatment effectively inhibited these factors and enhanced the expression of anti-inflammatory cytokines, such as IL-10 and IFN-γ. Protein and mRNA analysis revealed that PEITC could significantly suppress the activation of TLR3, TICAM-1, p65, JAK/STAT, and MAPK signaling, and promote TRAF3 expression. In subsequent animal experiments, we induced acute neuroinflammation in mice with Poly (I:C) and found that PEITC effectively alleviated cortical inflammation, reduced Iba1 expression, and guided microglia to switch from a pro-inflammatory M1 to an anti-inflammatory M2 phenotype. In summary, this study confirms that PEITC can modulate the microglial activation and neuroinflammation induced by viral-like stimuli and participates in the regulation of multiple immune-related signaling pathways. This provides a potential drug candidate and research foundation for developing therapeutic strategies for virus-infection-related neuroinflammatory diseases in the future. - Source: PubMed
Publication date: 2026/07/09
Lan Yi-ChingXiao Yan-RuHsieh Yow-WenCheng Yih-DihPeng Shu-FenChueh Fu-ShinLee Hsu-TungHsieh Yu-ShengJiang Wei-ChengHsieh Wen-TsongChou Yu-Cheng