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ICAM1 — POLDIP2

Text-mined interactions from Literome

Arnold et al., J Immunol 2005 : The virus induced ICAM-1 up-regulation was dependent on protein kinase C and A, PI3K, and p38 MAPK activity
Chen et al., Hypertension 2006 (Necrosis) : Inhibiting the phosphatidylinositol 3-kinase and p38 mitogen activated protein kinase pathways blocked both expression of ICAM-1 and phagocytosis, whereas inhibition of the P42/44 mitogen activated protein kinase pathway blocked only ICAM-1 expression
Wang et al., J Immunol 2006 : ICAM-1 engagement by HRV and cross linking Abs also induced phosphorylation of p38 in a Syk dependent manner, and conversely, knockdown of Syk by short interfering ( si ) RNA substantially diminished p38 activation and IL-8 gene expression
Kwon et al., J Korean Med Sci 2007 (Leukemia) : However, neither p38 MAP kinase inhibitor nor MEK inhibitor prevented HDM induced ICAM-1 expression in EoL-1 cells
Shen et al., FEBS J 2008 : Lipopolysaccharide evoked activation of p38 and JNK leads to an increase in ICAM-1 expression in Schwann cells of sciatic nerves
Hsu et al., J Cell Physiol 2011 : Furthermore, resistin increased the expression of intercellular adhesion molecule-1 ( ICAM-1 ) and vascular cell adhesion molecule-1 ( VCAM-1 ) by HUVECs and these effects were also p38MAPK dependent
Watanabe et al., Acta Med Okayama 2011 (Diabetes Mellitus, Experimental...) : Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK ... We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions