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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
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 results of cell adhesion and western blotting assays demonstrated that arachidin-1 attenuated tumor necrosis factor (TNF)-alpha (show TNF Proteins)-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.
15-LOX-1 expression in colon and prostate cancer cells leads to reduced angiogenesis. These changes could be mediated by an increase in the expression of both ICAM-1 and the anti-angiogenic protein TSP-1.
Single nucleotide polymorphisms in ICAM1 (rs1799969) and SERPINB2 (rs6103) genes were found to be protective against thalidomide-induced peripheral neuropathy (TiPN). In children with inflammatory bowel disease, TiPN is common but mild and generally reversible. Cumulative dose seems to be the most relevant risk factor, whereas polymorphisms in genes involved in neuronal inflammation may be protective.
analysis of aberrant DNA methylation (show HELLS Proteins) and hydroxymethylation of the ICAM1 gene promoter in the thyrocytes of Autoimmune Thyroiditis patients
There was a significant correlation between the level of VEGF (show VEGFA Proteins) and ICAM1 and histologic type of tumors in invasive through in situ tumors
Authors demonstrate that the membrane-bound ICAM-1 isoform is necessary and sufficient to promote inflammation-dependent extracellular matrix contraction, which favors cancer cell invasion. Indeed, ICAM-1 mediates generation of acto-myosin contractility downstream of the Src (show SRC Proteins) kinases in stromal fibroblasts.
Thrombin (show F2 Proteins) activated platelet releasing exosomes convey miRNA between cells. miRNA-223 regulates the expression of molecules adhesion including ICAM-1. miRNA-223 downregulated ICAM-1 mainly by impacting NF-kappaB (show NFKB1 Proteins) and the MAPK (show MAPK1 Proteins) pathway.
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