ICAM-1, human recombinant proteins
- Known as:
- ICAM-1, H. sapiens Rec. proteins
- Catalog number:
- 7161-50
- Product Quantity:
- 50 μg
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- ICAM-1 human recombinant proteins
Related genes to: ICAM-1, human recombinant proteins
- 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: ICAM-1, human recombinant proteins
Related articles to: ICAM-1, human recombinant proteins
- Renal ischemia/reoxygenation triggers uremic encephalopathy (UE), culminating in cognitive and neural derangements. Despite its neuroprotective functions, the hippocampal repercussion of the estrogen receptor G protein-coupled estrogen receptor 1 (GPER1) in UE remains uncharted, alongside the prospective involvement of RUNX2. In Silico virtual screening suggested that prunetin (PRU) may activate GPER1 and inhibit RUNX2. To validate these findings in vivo, male Sprague Dawley rats were allocated into five groups: placebo-surgery (PS), PRU-treated PS, untreated UE, PRU-treated UE, and UE pretreated with G-15 (a selective GPER1 blocker) before PRU. Biochemically, PRU significantly restored hippocampal structure and behavioral functions impaired by UE, reduced serum IS levels, and replenished GPER1 expression. Additionally, it suppressed p-AKT, p-GSK3β, RUNX2, TLR4, and NF-κB, while enhancing cell survival by silencing the necroptotic signal (TICAM1/RIPK1/RIPK3/MLKL) and restoring caspase-8. PRU also counteracted mitochondrial dysfunction by downregulating PGAM5 and p-DRP-1. Crucially, these beneficial effects were nullified by G-15, confirming the role of activated GPER1 in mediating PRU's therapeutic effects. Collectively, PRU-induced GPER1 orchestrated neural integrity signal UE/AKT/GSK-3β/RUNX2, inflammatory axis UE/TLR-4/NF-κB, necroptosis pathway (TICAM1/RIPK1/RIPK3/MLKL), preventing mitochondrial dysfunction by suppressing the PGAM5/DRP-1 cue. These findings highlight the therapeutic potential of PRU in treating UE-related hippocampal damage through GPER1 activation. - Source: PubMed
Hamed Ahmed BFawzy Iten MAbdallah Dalaal MAbulfadl Yasmin SAhmed Kawkab AEl-Abhar Hanan S - Intestinal homeostasis depends critically on the dynamic interplay between gut microbiota, epithelial barriers, and host immunity, dysregulation of this triad can initiate inflammatory cascades. Ferulic acid and its derivative N-Feruloylserotonin demonstrate significant anti-inflammatory activity, though their intestinal protective effects and mechanisms require further elucidation. Therefore, this study examined how these compounds mitigate lipopolysaccharide (LPS)-induced acute inflammation through integrated modulation of the gut microbiome, serum metabolome, and transcriptional networks. Our findings reveal that both compounds, attenuated LPS-induced intestinal pathology in murine models, suppressed pro-inflammatory cytokine expression, elevated beneficial metabolites including 1-naphthalenesulfonic acid, enriched probiotic taxa (Ruminococcaceae, Muribaculaceae, Lachnospiraceae, Bifidobacteriaceae, Prevotellaceae, Roseburia, Blautia, and Butyricicoccus), and suppressed pathobionts (Proteobacteria, Gammaproteobacteria, Enterobacterales, and Bacillus). Transcriptomic profiling further implicated modulation of antigen processing and presentation, NF-κB signal pathway, MAPK signal pathway, and PI3K-Akt signal pathway. Key regulatory targets identified include: Pik3cd, H2-DMb1, H2-Oa, Kdr, Fgfr3, Il1r2, Rac, Irak4, Traf6, Ticam1, Rip1, and Rip3. This work establishes a mechanistic foundation for deploying ferulic acid and N-Feruloylserotonin in intestinal health preservation and inflammatory disease prevention, while providing novel insights into microbiota-homeostasis crosstalk. - Source: PubMed
Publication date: 2025/07/22
Hu XiangdongHan XuebingLiu GangGuan GuipingXia Chenmei - Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality and morbidity worldwide. Chronic inflammation of the endothelium is a pivotal process in the pathogenesis of ASCVD. Therefore, the identification of pro-atherogenic gene expression and subsequent screening out of potential therapeutic agents for vascular inflammation is an attractive issue. The TICAM1 and IRF3 genes were identified as susceptibility genes whose expression was upregulated in lipopolysaccharide (LPS)-induced vascular inflammation. Cilostazol was found to be the most potential bioactive drug for the TICAM1 proteins. Cilostazol pretreatment also increased autophagy and decreased necroptosis and NLRP3/NLRP6 inflammasome formation, as well as the pro-inflammatory cytokine interleukin-1β, in vitro and in vivo. Additionally, cilostazol significantly attenuated the TNF-α-induced elevation in circulating adhesion molecules. Furthermore, cilostazol treatment markedly reduced aortic wall thickening in TNF-α-challenged mice. After experiments into mechanistic understanding, we found that the candidate drug cilostazol reduces vascular inflammation and possibly atherosclerosis progression. Therefore, this study can offer broader evidence of cilostazol for treating individuals with ASCVD or at high risk of ASCVD. Further prospective clinical trials are warranted to confirm its application and effectiveness. - Source: PubMed
Publication date: 2025/06/17
Chiu Hui-WenShih Chun-CheHuang Hung-JinHuang Tzu-HsuanSung Li-Chin - Toll-like receptors (TLRs) play critical roles in pain modulation and immune responses. Polyinosinic-polycytidylic acid (Poly-IC), a TLR3-specific ligand, has shown promise in exerting neuroprotective effects, as it mitigates inflammation in several diseases. Considering that sterile neurogenic inflammation is involved in the pathogenesis of migraine, we explored the impact of Poly-IC on episodic migraine treatment and the potential mechanisms involved. - Source: PubMed
Hong YeMa MengmengLi ChanglingZhang YangLi YanboChen NingFang JinghuanHe Li - Human papillomavirus (HPV) is a major etiological agent of both malignant and benign lesions, with high-risk types, such as HPV16 and HPV18, being strongly linked to cervical cancer, while low-risk types like HPV11 are associated with benign conditions. While viral proteins such as E6 and E7 are well-established regulators of immune evasion, the role of E1 in modulating the host antiviral responses remains insufficiently characterized. This study investigates the immunomodulatory functions of HPV16 and HPV11 E1 in suppressing innate antiviral immune signaling pathways. Through a combination of RT-qPCR and luciferase reporter assays, we demonstrate that E1 suppresses the production of interferons and interferon-stimulated genes triggered by viral infections and the activation of RIG-I/MDA5-MAVS, TLR3-TRIF, cGAS-STING, and JAK-STAT pathways. Co-immunoprecipitation assays reveal that E1 interacts directly with key signaling molecules within these pathways. E1 also impairs TBK1 and IRF3 phosphorylation and obstructs the nuclear translocation of IRF3, thereby broadly suppressing IFN responses. Additionally, E1 disrupts the JAK-STAT pathway by binding STAT1, which prevents the assembly and nuclear localization of the ISGF3 complex containing STAT1, STAT2, and IRF9, thereby further diminishing antiviral response. These findings establish E1 as a pivotal regulator of immune evasion and suggest its potential as a novel therapeutic target to enhance antiviral immunity in HPV-associated diseases. - Source: PubMed
Publication date: 2025/04/22
Li Jin-XinZhang JingLi Cheng-HaoLi Yun-FangChen Hui-MinLi TaoZhang QingKong Bei-HuaWang Pei-Hui