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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
miR-335-5p could target 3'UTR of ICAM-1 and inhibit its expression, preventing invasion and metastasis of thyroid cancer cells.
AGEs increase IL-6 and ICAM-1 expression via the RAGE, MAPK and NF-kappaB pathways in HGFs and may exacerbate the progression of the pathogenesis of periodontal diseases.
Our meta-analyses provide no evidence of the association of ICAM-1 rs5498 with diabetic retinopathy in type 2 diabetic patients.
CORM-2 inhibits P. aeruginosa-induced PGE2/IL-6/ICAM-1 expression and lung inflammatory responses by reducing the Reactive Oxygen Species generation and the inflammatory pathways.
Smooth muscle cell-derived bioactive soluble factors may stimulate the ICAM-1 expression of cocultured endothelial cells, possibly leading to leukocyte migration into the subendothelial space.
These results together with the authors' previous study, have identified that CNOT1 provides a platform for the recruitment of TTP and CNOT7, and is involved in TTPmediated ICAM1 and IL8 mRNA decay.
ICAM-1 expression is not significantly linked to metastatic disease in pancreatic ductal adenocarcinoma.
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 and IL-10 treatment can affect the expression of ICAM-1 and CD31 in human coronary artery endothelial cells.
not a specific screening marker for pulmonary arterial hypertension in systemic sclerosis
The ICAM-1 expression level determines the susceptibility of human endothelial cells to simulated microgravity.
the combination of IL-6 -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+ 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 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 compared to sICAM-1 in differentiating subjects with CNS brain tumors from non-tumoral subjects.
Patient-derived ATC 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 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)-causing and non-AHC strains.
The results of cell adhesion and western blotting assays demonstrated that arachidin-1 attenuated tumor necrosis factor (TNF)-alpha-induced monocyte/EC adhesion and intercellular adhesion molecule-1 (ICAM-1) expression
anthropometric and physiological parameters do not affect the response of ICAM-1 to exercise in healthy men.
The present study demonstrated that IL-1b may induce ICAM-1 expression, thus enhancing the cohesion between mesenchymal stem cells and endothelial progenitor cells via the p38 MAPK 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) and lymphoblast transformation test (LTT) tests.
The results showed that MOVACs transfected with pCMV5-HA-RKIP significantly inhibited TNF-a induced mRNA and protein expression of ICAM-1 and VCAM-1.
Endotoxaemia enhanced early venous thrombosis occurs in a TLR-4 and ICAM-1 dependent fashion, and is potentiated by neutropenia.
Neither the lack of CD36 nor the deletion of the smac 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 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 colocalized with its substrates at the leading edge of cells migrating on surfaces coated with the LFA-1 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 and beta-catenin signaling, increased epithelial-cell proliferation, and wound healing.
Blocking CD54 inhibited NK cell-mediated cytotoxicity of the GM-CSF-stimulated Flt3 ligand conventional dendritic cells. NK cell-mediated lysis of GM-CSF-stimulated cDCs was, in part, a result of increased expression of CD54.
These results indicate that, whereas T cells use ICAM-1 and -2 for temporary pulmonary entrapment, neutrophils get sequestered and extravasate into inflamed lungs independent of ICAMs.
This study indicates that the ANG II effects are, in part, mediated or triggered by Gal-3 together with the related intercellular signaling (ICAM-1 and IL-6), leading to cardiac inflammation and fibrosis.
Data suggest CKIP1 (casein kinase 2 interacting protein-1) plays role in resistance to oxidative stress in glomerular mesangial cells in development of diabetic nephropathy; mechanisms appear to include down-regulation of expression of ICAM1 (intercellular adhesion molecule-1) and fibronectin plus activation of Nrf2/ARE (nuclear factor E2-related factor 2/antioxidant response element) antioxidative stress pathway.
ICAM1 regulates pathological cardiac remodeling by mediating proinflammatory leukocyte infiltration in the left ventricle and cardiac fibrosis and dysfunction.
Its antiatherogenic impact might be associated with a suppressed adhesion to the endothelium due to down-regulation of endothelial ICAM-1 expression.
Luteolin may inhibit tumor angiogenesis and tumor cell proliferation by down-regulation of LFA- 3 and PCNA and up-regulation of ICAM-1 in tumor tissue of tumor-bearing mice, thereby achieving its anti-tumor effect.
our results further highlight the pleiotropic role of ICAM-1 in T-cell-dependent immune responses, with a major role in Treg cell development and suppressive function.
the present results shed light on regulation of expression and function of ICAM-1 on neutrophils and identify it as an additional regulator of neutrophil effector responses in host defense.
we identified intracellular adhesion molecule (ICAM)-1, through fibrinogen binding, as a previously unreported mediator of platelet-monocyte interactions
ADMA has potent adverse effects on cell proliferation, intracellular ROS generation, cell permeability, levels of ICAM-1, and the tight-junction protein occludin
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 and ICAM-1 by inhibiting the phosphorylation of Mitogen-Activated Protein Kinases and the activation of NF-kappaB in lipopolysaccharides treated porcine iliac artery endothelial cells.
Data show that all five molecules, BNP, ICAM-1, TNF-alpha, VCAM-1 and IL-6, quickly and reliably signaled adverse interactions.
Altered shear stress stimulates upregulation of endothelial VCAM-1 and ICAM-1 in a BMP-4- and TGF-beta1-dependent pathway.
ICAM1 and IL10 were upregulated in ventilator-induced lung injury. Nuclear transcription factor AP-1 may be responsible for this upregulation.
Hepatocellular glycogen 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