Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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
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.
Data suggest that obese children/adolescents have increased circulating biomarkers of endothelial dysfunction (here, ICAM1) and early signs of renal damage, similarly to children/adolescents with type 1 diabetes (T1D), confirming obesity to be a cardiovascular risk factor as is T1D.
ICAM-1 (and IL-17 (show IL17A Proteins)) polymorphisms showed significant association with Guillian-Barre syndrome.
Airway ICAM-1 expression is markedly upregulated in CAL (show FBLIM1 Proteins) group, which could be crucial in rhinoviral and NTHi infections. The parenchymal ICAM-1 is affected by smoking, with no further enhancement in CAL (show FBLIM1 Proteins) subjects.
Atorvastatin strengthens Skp2 binding to FOXO1 or ICAM1, leading to ubiquitination and degradation. Skp2-dependent ubiquitination of major pathogenic molecules is the key mechanism for statin's protective effect on endothelial function in diabetes.
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)).
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.
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.
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