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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
Augmented expression of endothelial adhesion molecules ICAM1/VCAM1 (show VCAM1 Proteins) is involved in the pathophysiology of patients with antiphospholipid syndrome.
CD133(+) CD44 (show CD44 Proteins)(+) CD54(+) cellular subpopulation of circulating tumor cells has a prognostic value in colorectal cancer patients with liver metastasis, especially in the survival of CRC (show CALR Proteins) patients with liver metastasis who did not undergo surgical treatment for metastasis.
Data suggest that the residue volume at phenylalanine (Phe) in alpha1-helix is critical for alpha(L)/beta(2) integrin (CD49a (show ITGA1 Proteins)/CD18 (show ITGB2 Proteins)) activation and binding with soluble/immobilized ICAM1 (intercellular cell adhesion molecule 1 (show CADM1 Proteins)).
Elevated serum uric acid concentration is significantly associated with inflammation of maternal systemic vasculature as indicated by increased TNF-alpha (show TNF Proteins) and ICAM-1 expression in women with preeclampsia.
Data indicate that CDH11, ICAM1 and CLDN3 (show CLDN3 Proteins) were overexpressed in tumors when compared to normal esophagus, normal gastric and non-dysplastic Barrett's.
High levels of serum ICAM-1 was associated with the development of multiple organ failure . High levels of VCAM-1 (show VCAM1 Proteins) was associated with both multiple organ failure and in-hospital mortality.
matrix stiffness-dependent ICAM-1 clustering is an important regulator of vascular inflammation
PD increased CKIP-1 (show PLEKHO1 Proteins) and Nrf2 (show GABPA Proteins) levels in the kidney tissues as well as improved the anti-oxidative effect and renal dysfunction of diabetic mice, which eventually reversed the up-regulation of FN and ICAM-1
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.
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.
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.
Blocking CD54 inhibited NK cell-mediated cytotoxicity of the GM-CSF (show CSF2 Proteins)-stimulated Flt3 ligand (show FLT3LG Proteins) conventional dendritic cells. NK cell-mediated lysis of GM-CSF (show CSF2 Proteins)-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 (show AGT Proteins) effects are, in part, mediated or triggered by Gal-3 (show LGALS3 Proteins) together with the related intercellular signaling (ICAM-1 and IL-6 (show IL6 Proteins)), 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 (show FN1 Proteins) plus activation of Nrf2 (show NFE2L2 Proteins)/ARE (nuclear factor E2-related factor 2/antioxidant response element) antioxidative stress pathway.
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