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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