Recombinant Human ICAM2 /CD102 Protein
- Known as:
- Recombinant Human ICAM2 /CD102 Protein
- Catalog number:
- ic-799
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human ICAM2 /CD102 Protein
Related genes to: Recombinant Human ICAM2 /CD102 Protein
- Gene:
- ICAM2 NIH gene
- Name:
- intercellular adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- CD102
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-06
- Date modifiied:
- 2015-08-28
Related products to: Recombinant Human ICAM2 /CD102 Protein
Related articles to: Recombinant Human ICAM2 /CD102 Protein
- Pediatric sepsis is increasingly recognized as a syndrome involving immune-vascular dysregulation. However, most pediatric biomarker studies focus on individual molecules rather than coordinated patterns of leukocyte-endothelial activation. This study aimed to evaluate whether children diagnosed with sepsis within 48 h of admission showed a coordinated soluble adhesion-molecule activation profile measured at enrollment. This prospective cohort study included 144 children aged 1-60 months with suspected infection enrolled at Dong Nai Children's Hospital, Vietnam, from May 2021 to October 2022. Blood samples were collected at enrollment. Sepsis was classified according to the 2005 International Pediatric Sepsis Consensus Conference (IPSCC) criteria within 48 h of admission. Twelve soluble adhesion molecules were measured using a multiplex immunoassay. A composite adhesion activation score was derived by log2 transformation, z-score standardization, and averaging across the 12 markers. Principal component analysis (PCA) was used as an exploratory method to summarize the shared variation across the adhesion-molecule panel. C-reactive protein (CRP) was included as a routinely available inflammatory comparator. Among 144 children, 32 (22.2%) were diagnosed with sepsis within 48 h of admission. Individual marker discrimination was strongest for L-selectin (area under the receiver operating characteristic curve [AUC] 0.883), followed by soluble vascular cell adhesion molecule-1 (sVCAM-1; AUC 0.855), intercellular adhesion molecule-3 (ICAM-3; AUC 0.838), P-selectin glycoprotein ligand-1 (PSGL-1; AUC 0.836), E-selectin (AUC 0.819), and intercellular adhesion molecule-2 (ICAM-2; AUC 0.819). CRP also differed between children with and without sepsis but had a lower AUC than the leading adhesion molecules in descriptive ROC analyses. The composite adhesion activation score was strongly associated with sepsis (odds ratio 7.95 per 1-standard deviation increase; 95% confidence interval 3.44-18.40; < 0.001) and showed good discrimination (AUC 0.855; 95% confidence interval 0.776-0.931). The first principal component explained 70.0% of biomarker variance, consistent with coordinated elevation of correlated adhesion molecules. In this prospective Vietnamese pediatric cohort, children diagnosed with sepsis within 48 h of admission showed coordinated elevation of soluble adhesion molecules measured at enrollment. These findings support the biological relevance of leukocyte-endothelial activation in pediatric sepsis. However, the adhesion-molecule activation profile should be considered exploratory and hypothesis-generating, requiring external validation and further evaluation against simplified, clinically feasible biomarker approaches. - Source: PubMed
Publication date: 2026/06/09
Liem Bui ThanhThien Chu VanNghia Nguyen TrongPhong Le AnhDinh Ngo NhuLuan Nguyen HuyNguyen Phung Nguyen The - Inflammatory bowel disease (IBD) is a chronic and recurrent gastrointestinal disease, the pathogenesis of which has not been fully elucidated. Increasing evidence suggests that the disorder of mitochondrial metabolism is closely related to the pathogenesis of IBD, but its specific regulatory network and key genes remain to be further investigated. IBD-related transcriptome datasets (GSE3365 and GSE75214) and single-cell sequencing dataset (GSE134809) were obtained from the Gene Expression Omnibus database. Differentially expressed genes and hub genes were identified through differential expression analysis and weighted gene co-expression network analysis, and candidate genes were obtained by intersecting these with mitochondrial metabolism-related genes, followed by functional enrichment analysis. Machine learning algorithms were used to screen key genes and construct risk prediction models. Additionally, analysis of GSE134809 single-cell data identified characteristic cell types and expression distribution of key genes in IBD and explored communication between different cell types. Furthermore, immune cell infiltration, competitive endogenous RNA (ceRNA) network, and transcription factor prediction were performed. Finally, the diagnostic performance of key genes was validated in GSE75214 and reverse transcription-quantitative polymerase chain reaction. Two key genes, mitochondrial ribosomal protein L35 () and , were identified, which were downregulated in IBD, and had good diagnostic potential. Single-cell analysis revealed that key genes were predominantly highly expressed in mononuclear phagocyte (MNP) cells. MNP cells communicated with other cells through receptor ligands including MIF-(CD74 + CXCR4), MDK-SDC1, and ITGB2-ICAM2, which are complexly related to mitochondrial metabolism. With the progression of IBD, infiltration levels of resting natural killer cells, naive B cells, M2 macrophages, and naive CD4 T cells decreased, and correlations between different cells continuously changed. A ceRNA network centered on XIST, hsa-miR-103a-3p, and was constructed. Additionally, therapeutic drugs targeting key genes were predicted, including cimetidine, eugenol, chlortetracycline, vincristine, irinotecan, bisacodyl, and sulpiride, with molecular docking validating high affinity between these drugs and key targets. This study constructed a multiomics integrated analysis strategy and identified and as potential markers and therapeutic targets, providing new insights for the diagnosis and treatment of IBD. - Source: PubMed
Publication date: 2026/06/15
Li HaoWu XichuanWu QingpingWang Jian - Idiopathic myocardial fibrosis (IMF) is a prevalent and life-threatening condition in captive chimpanzees (). Ante-mortem diagnosis remains challenging due to the limitations of current veterinary diagnostics. This study aimed to identify and validate circulating serum protein biomarkers for the detection of IMF. - Source: PubMed
Publication date: 2026/05/19
Jarvis Martin RachelBaiker KerstinMoittié SophieDobbs PhillipaWhite KateLiptovszky MatyasGrant Melissa M - Megakaryocytes (MKs) and low-density granulocytes (LDGs) are implicated in immune dysregulation and vascular pathology in autoimmune diseases (ADs), yet their precise subsets and pathological interactions remain poorly defined. We aimed to characterize MK and LDG subpopulations and elucidate their potential intercellular communication in ADs using single-cell transcriptomic analysis. - Source: PubMed
Publication date: 2026/05/10
Chen ShaoqiFan YuSu MiaotongLin YuqingZheng ShaoyuZhou ZexuanZhang WeijinLin JianqunHu ShijianMatucci-Cerinic MarcoFurst Daniel EZhang GuohongWang Yukai - Acquired endocrine resistance in ER breast cancer (BC) involves metabolic reprogramming, yet key drivers are unclear. Multi-omics of endocrine-resistant BC revealed upregulated oxidative phosphorylation (OXPHOS) and identified intercellular adhesion molecule 2 (ICAM2) as a biomarker of high-OXPHOS cells. ICAM2-positive cells were significantly enriched in resistant tumors and predicted poor survival, and were functionally essential for maintaining resistance and promoting metastasis in vivo. Mechanistically, ICAM2 binds dynein light chain DYNLT3 and the mitochondrial complex I subunit MT-ND2, thereby facilitating dynein-mediated mitochondrial trafficking and further modulating the assembly of mitochondrial complex I. Disrupting this interaction through ICAM2 knockdown or dynein inhibition (Ciliobrevin D) effectively suppressed OXPHOS activity. Importantly, ERα inhibition alleviates the transcriptional repression of ICAM2 by ERα. Therapeutically, combining the complex I inhibitor IACS-10759 with fulvestrant potently inhibited both tumor growth and metastasis. Collectively, these findings reveal that ICAM2 drives endocrine resistance via dynein-dependent OXPHOS activation, revealing a targetable axis in refractory ER BC. In summary, we establish ICAM2 as a novel biomarker and driver of endocrine resistance in ER⁺ breast cancer. ICAM2⁺ cancer cells-enriched in treatment-resistant tumors-maintain elevated OXPHOS by assembling a functional complex with dynein and mitochondrial Complex I, thereby promoting mitochondrial trafficking. Disruption of this axis, either through ICAM2 depletion or Complex I inhibition, re-sensitizes tumors to therapy, revealing a targetable metabolic dependency in resistant disease. - Source: PubMed
Publication date: 2026/05/18
Chen SiWu ShiyiHu JiajieLiu BohanLiu YutingYang SiyueTang FenHe YiqingLiu QinqingLiu YiwenDu YanZhang GuoliangGuo QianGao FengYang Cuixia