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Human ICAM-1 Protein expressed in Human Cells - ABIN2002637
Bhalla, Chugh, Mehrotra, Rathore, Tousif, Prakash Dwivedi, Prakash, Kumar Samuchiwal, Kumar, Kumar Singh, Ghanwat, Kumar, Das, Mohmmed, Malhotra, Ranganathan: Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum. in Nature communications 2015
In conclusion, this meta-analysis indicates that ICAM-1 gene rs5498 polymorphism decreases the risk of CAD
Data suggest that serum levels of soluble ICAM1 are higher in young adults with reduced physical activity as compared to young adults who participate in optimal physical activity. This study was conducted in Bulgaria with medical and dental students aged 20 +/-2 years.
TNF-alpha (show TNF Proteins) and IL-10 (show IL10 Proteins) treatment can affect the expression of ICAM-1 and CD31 (show HBA1 Proteins) in human coronary artery endothelial cells.
The ICAM-1 expression level determines the susceptibility of human endothelial cells to simulated microgravity.
the combination of IL-6 (show IL6 Proteins) -572C/G and ICAM-1 K469E polymorphisms have a synergistic effect on the onset of Sudden sensorineural hearing loss.
Peripheral blood lymphocyte subsets in patients with lung cancer are different from those in healthy people, and circulating CD44 (show CD44 Proteins)+ and CD54+ lymphocytes seem to be a promising criterion to predict survival in lung cancer patients undergoing chemotherapy
serum ICAM-1 levels were associated with type 2 diabetes mellitus with microalbuminuria leading to severity of diabetic kidney disease.
Serum CCL2 (show CCL2 Proteins) and sICAM-1 concentrations were significantly decreased in CNS tumors in comparison with the comparative group. Among proteins tested in the serum, a higher area under the ROC curve (AUC) revealed CCL2 (show CCL2 Proteins) compared to sICAM-1 in differentiating subjects with CNS brain tumors from non-tumoral subjects.
Patient-derived ATC (show SRPK1 Proteins) cells overexpressed ICAM-1 and were largely eliminated by autologous ICAM-1 CAR T cells in vitro and in animal models. Our findings are the first demonstration of CAR T therapy against both a metastatic, thyroid cancer cell line and advanced ATC (show SRPK1 Proteins) patient-derived tumors that exhibit dramatic therapeutic efficacy and survival benefit in animal studies
Data indicate ICAM-1 as an essential receptor for both acute hemorrhagic conjunctivitis (AHC (show NR0B1 Proteins))-causing and non-AHC (show NR0B1 Proteins) strains.
The present study demonstrated that IL-1b (show IL1B Proteins) may induce ICAM-1 expression, thus enhancing the cohesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK (show MAPK14 Proteins) signaling pathway.
ICAM-1 overexpressing Mesenchymal Stem Cells could suppress Dendritic Cells maturation according to co-culture methods and suppress the T cell immune response according to the mixed lymphocyte response (MLR (show RPSA Proteins)) and lymphoblast transformation test (LTT) tests.
The results showed that MOVACs transfected with pCMV5-HA-RKIP (show PEBP1 Proteins) significantly inhibited TNF-a (show TNF Proteins) induced mRNA and protein expression of ICAM-1 and VCAM-1 (show VCAM1 Proteins).
Endotoxaemia enhanced early venous thrombosis occurs in a TLR-4 (show TLR4 Proteins) and ICAM-1 dependent fashion, and is potentiated by neutropenia.
Neither the lack of CD36 (show CD36 Proteins) nor the deletion of the smac (show DIABLO Proteins) gene from Plasmodium chabaudi significantly impacted on acute-stage pathology or parasite sequestration. By contrast, in the absence of ICAM-1, infected animals experience less anaemia and weight loss, reduced parasite accumulation in both spleen and liver and higher peripheral blood parasitaemia during acute stage malaria.
Data show that intercellular adhesion molecule 1 (ICAM-1) and ICAM-2 (show ICAM2 Proteins) on B cells are essential for long-lasting cognate T follicular helper (Tfh)-B cell interactions and efficient selection of low-affinity B cell clones for proliferative clonal expansion
in T cells, PI3Kdelta attenuates the activation of Rac1, but sustains the activation of Rap1.
PTPN22 (show PTPN22 Proteins) colocalized with its substrates at the leading edge of cells migrating on surfaces coated with the LFA-1 (show ITGAL Proteins) ligand intercellular adhesion molecule-1 (ICAM-1).
These results suggest that SHP-2-via association with ICAM-1-mediates ICAM-1-induced Src activation and modulates VE-cadherin switching association with ICAM-1 or actin, thereby negatively regulating neutrophil adhesion to endothelial cells and enhancing their transendothelial migration.
Following transepithelial migration, neutrophils adhesion to ICAM-1 resulted in activation of Akt (show AKT1 Proteins) and beta-catenin (show CTNNB1 Proteins) signaling, increased epithelial-cell proliferation, and wound healing.
ADMA has potent adverse effects on cell proliferation, intracellular ROS (show ROS1 Proteins) generation, cell permeability, levels of ICAM-1, and the tight-junction protein occludin (show OCLN Proteins)
Neutrophil lung infiltrations in porcine reproductive and respiratory syndrome virus infection infected animals is both ICAM-1 dependent and independent.
Chitosan oligosaccharides downregulate the expression of E-selectin (show SELE Proteins) and ICAM-1 by inhibiting the phosphorylation of Mitogen-Activated Protein Kinases and the activation of NF-kappaB (show NFKB1 Proteins) in lipopolysaccharides treated porcine iliac artery endothelial cells.
Data show that all five molecules, BNP, ICAM-1, TNF-alpha (show TNF Proteins), VCAM-1 (show VCAM1 Proteins) and IL-6 (show IL6 Proteins), quickly and reliably signaled adverse interactions.
Altered shear stress stimulates upregulation of endothelial VCAM-1 (show VCAM1 Proteins) and ICAM-1 in a BMP-4 (show BMP4 Proteins)- and TGF-beta1 (show TGFB1 Proteins)-dependent pathway.
ICAM1 and IL10 (show IL10 Proteins) were upregulated in ventilator-induced lung injury. Nuclear transcription factor AP-1 (show JUN Proteins) may be responsible for this upregulation.
Hepatocellular glycogen (show GYS1 Proteins) decreases the expression of ICAM-1 mRNA of hepatic stellate cells.
This gene encodes a cell surface glycoprotein which is typically expressed on endothelial cells and cells of the immune system. It binds to integrins of type CD11a / CD18, or CD11b / CD18 and is also exploited by Rhinovirus as a receptor.
intercellular adhesion molecule 1
, intercellular adhesion molecule 1-like
, cell surface glycoprotein P3.58
, intercellular adhesion molecule 1 (CD54), human rhinovirus receptor
, major group rhinovirus receptor
, leukocyte adhesion molecule