Ask about this productRelated genes to: ICAM1 antibody
- 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: ICAM1 antibody
Related articles to: ICAM1 antibody
- Xuesaitong injection has been explored as an off-label adjuvant therapy for acute pancreatitis in China, but its efficacy and safety remain uncertain. This systematic review and meta-analysis evaluated Xuesaitong injection combined with conventional therapy for acute pancreatitis. - Source: PubMed
Publication date: 2026/07/29
Fang YangbinChen XinCai LuoyangHan ZhenMa ZhengranLi LiGan ZhenkunLiu TaoZuo ZhengWang Yan - Glycyrrhizic acid (GL), a natural triterpenoid glycoside extracted from the "medicine food homology" herb L., exhibits potent anti-atherosclerotic effects; yet its underlying mechanisms remain unclear due to its poor oral bioavailability. The gut microbiota plays a pivotal role in the development of atherosclerosis (AS). In this study, the microbiota-dependent anti-AS effects of GL were evaluated in high-fat diet (HFD)-fed mice using antibiotic depletion and fecal microbiota transplantation (FMT). Integrated metagenomic and metabolomic analyses were performed to identify the key bioactive microbial metabolite. Further in vivo and in vitro experiments, including co-immunoprecipitation and dual-luciferase reporter assays, were utilized to elucidate the underlying molecular mechanisms. It was demonstrated that oral administration of GL alleviated AS in a microbiota-dependent manner by reversing gut dysbiosis, improving intestinal barrier function, and reducing pro-inflammatory lipopolysaccharide (LPS) levels. GL shifted intestinal tryptophan metabolism toward bacterial-derived indole-3-lactic acid (ILA) production, suppressing LPS-induced vascular endothelial adhesion dysfunction by activating the aryl hydrocarbon receptor (AhR). Mechanistically, ILA-activated AhR interacted with the NF-κB subunit p65 in the cytoplasm, effectively preventing the nuclear translocation of p65 and suppressing the promoter activities of adhesion molecules ( and ), resulting in the amelioration of HFD-induced AS. These findings elucidate the microbiota-dependent mechanism of orally administered GL against AS, and highlight the therapeutic potential of targeting the ILA-AhR-p65 axis in the vascular endothelium as a strategy for AS. - Source: PubMed
Publication date: 2026/07/27
Shen HaoranHuang ShuaiWang ZhiyuZhou SitongHuang LuluZhang HongjuanHan YanxingJiang JiandongGuo Huihui - Diabetic cataract (DC) is a lens-opacity complication of diabetes driven by hyperglycemia-related oxidative, apoptotic, metabolic, and epithelial-mesenchymal transition (EMT) pathways. This review evaluated the expression and mechanistic roles of long non-coding RNAs (lncRNAs) and lncRNA-related epitranscriptomic regulators in DC. - Source: PubMed
Publication date: 2026/08/12
Chen Kai-YangChan Hoi-ChunChan Chi-Ming - Sialic acid-binding Ig-like lectin-9 (Siglec-9) is a neutrophil inhibitory receptor. Prior studies have shown that sickle red blood cells (SS RBCs) abnormally engage neutrophil Siglec-9, suggesting that SS RBCs may not be able to effectively inhibit neutrophil activation. We examined SS RBC/Siglec-9 interactions and determined the effect of SS RBCs on Siglec-9 expression and neutrophil function. Using a novel monoclonal antibody-specific immobilization of erythrocyte antigen (MAIEA) assay, we demonstrated that SS RBCs have significantly decreased glycophorin A (GPA) and glycophorin B (GPB)-mediated binding to Siglec-9. Furthermore, exposure of healthy neutrophils to SS RBCs but not healthy AA RBCs induced shedding of Siglec-9 from neutrophil surfaces . , sickle cell disease (SCD) patients had fewer Siglec-9 positive neutrophils and elevated plasma soluble Siglec-9. Disruption of SS RBC/Siglec-9 interactions, both by desialylating RBCs and by blocking neutrophil Siglec-9, enhanced SS RBC-induced but not healthy AA RBC-induced neutrophil extracellular trap (NET) release. Finally, in a cohort of 32 SCD patients, soluble Siglec-9 was correlated with fetal hemoglobin (HbF), soluble intercellular adhesion molecule-1 (sICAM-1), and overall mortality. These studies demonstrate that unlike AA RBCs, SS RBCs not only directly activate neutrophils, but they also induce loss of neutrophil Siglec-9 and abnormally engage residual Siglec-9. Our findings suggest that neutrophil activation in SCD is a result of both direct activation and ineffective inhibition of neutrophils by SS RBCs. - Source: PubMed
Publication date: 2026/06/25
Lee Grace MBoyle KimberlyBatchvarova MilenaDelahunty MarthaTelen Marilyn J - Chimeric antigen receptor-engineered natural killer (CAR-NK) cells have emerged as a promising off-the-shelf platform for cancer immunotherapy, with a favorable safety profile in early clinical trials and potent antitumor activity demonstrated in relapsed/refractory (R/R) hematologic malignancies. However, their clinical efficacy in solid tumors remains severely limited by interconnected resistance mechanisms. In this review, we systematically dissect the pathological basis of CAR-NK therapy failure in solid tumors and propose an integrative cascade resistance framework that delineates three core bottlenecks: tumor microenvironment (TME)-mediated functional exhaustion, structural defects of non-natural killer (NK)-cell-adapted chimeric antigen receptors (CARs), and trogocytosis-driven immune escape. We further characterize the context-dependent regulatory roles of the natural killer group 2 member A-human leukocyte antigen E (NKG2A-HLA-E) immune checkpoint axis and the intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 (ICAM-1/LFA-1) adhesion pathway within this cascade model, with clear stratification of evidence strength across all mechanistic conclusions. Centered on the activating-inhibitory dual-module CAR (aCAR-iCAR) system, we summarize its design principles, preclinical validation status, and potential to mitigate cascade resistance, with explicit distinction between killer cell immunoglobulin-like receptor (KIR)-based (Level 1 evidence) and NKG2A-based (Level 2-3 evidence) inhibitory CAR backbones. We then outline an end-to-end artificial intelligence (AI)-driven rational design framework covering target screening, structural optimization, and signaling balance calibration, and introduce the AI-nanosymbiont concept as an exogenous synergistic strategy to address TME delivery barriers. Building on the molecular heterogeneity of solid tumors, we propose a four-subtype precision stratification framework to match tumor features with tailored therapeutic regimens, and summarize core translational challenges including manufacturing constraints, regulatory gaps, and safety considerations. Overall, this review provides a balanced, evidence-graded theoretical framework for next-generation CAR-NK development against solid tumors, and generates testable hypotheses for future mechanistic and clinical investigations. - Source: PubMed
Publication date: 2026/07/28
Ma ChenruZhuang YafeiHan SongchenLi ShupingDai Qiang