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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
Human ICAM-1 Protein expressed in HEK-293 Cells - ABIN2181238
Rothlein, Dustin, Marlin, Springer: A human intercellular adhesion molecule (ICAM-1) distinct from LFA-1. in Journal of immunology (Baltimore, Md. : 1950) 1986
Show all 2 Pubmed References
The serum soluble intercellular adhesion molecule-1 (sICAM-1) and IL-6 levels were significantly higher and showed a strong correlation in the patients with extrahepatic cholangiocarcinoma (EHC) than in the healthy volunteers. The high IL-6 group and the high sICAM-1 group showed poorer disease specific survival of EHC patients than those of the respective low groups.
Results found that loss of ICAM1 protein and mRNA expression was a strong prognosticator of diminished survival in BRAF/NRAS mutant melanoma.
Functional variants in ICAM-1 and TLR-4 genes were increasingly common in children with febrile UTIs with renal parenchymal involvement, but the ICAM-1 Glu469Lys (1462A/G) association was less evident.
The ICAM1 rs5498 might be a susceptible factor for T2D, but not T1D. And the allele and recessive models of ICAM1 rs5498 might be a risk factor in Asian population
This study included currently published evidence to comprehensively evaluate the influence of the rs5498 polymorphism within the ICAM1 gene on the genetic risk of multiple sclerosis. It was concluded that ICAM1 rs5498 may not be related to the risk of multiple sclerosis in Caucasian or Asian populations, which still merits further research.
No relationship was found between the ICAM-1 Lys469Glu polymorphism and systemic redox status in women with Gestational Diabetes.
Foxc2 attenuated adhesion of THP-1 cells to human umbilical vein endothelial cells by suppressing ICAM-1 expression.
Levels of antibodies that inhibit the binding of children's IE to the receptors ICAM-1, integrin alpha3beta1 and laminin increased with age. The breadth of antibodies that inhibit ICAM-1 and laminin adhesion (defined as the proportion of IE isolates whose binding was reduced by >/= 50%) also significantly increased with age.
On unbiased screening of serum cytokines and other markers in a diverse cohort, baseline soluble ICAM-1 is associated with hepatocellular carcinoma incidence.
Application of a novel risk score combining CEA/soluble ICAM-1 serum concentrations allows the identification of high-risk groups for poor survival in colorectal cancer patients.
results suggested that CRT could promote ICAM-1 expression in endothelial cells through PI3K/Akt/eNOS/p38 MAPK signaling mediated TTP accumulation, probably in an inactive form, which may provide a possible proinflammatory mechanism of CRT in rheumatoid arthritis.
ICAM1 rs5498 might be a risk factor for diabetic nephropathy in Caucasians and type 1 diabetes mellitus patients (meta-analysis).
rHDL also induced endothelial nitric oxide synthase eNOS S1177 phosphorylation in HMEC-1 but only when the particle contained sphingomyelin.
ICAM-1 may not be the sole mediator responsible for cytoadhesion in the brain.
Urothelial bladder cancer may suppress perforin expression in CD8+ T cells by an ICAM-1/TGFbeta2 mediated pathway
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 observations identify ICAM-1 as a novel regulator of Group 2 innate lymphoid cells.
High ICAM1 expression is associated with sepsis.
ICAM-1 augments myoblast adhesion and fusion.
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.
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