◀ Back to ICAM1

ICAM1 — WNK1

Text-mined interactions from Literome

Rahman et al., J Immunol 1999 : Thrombin induced p65 homodimer binding to downstream NF-kappa B site of the promoter mediates endothelial ICAM-1 expression and neutrophil adhesion
Ginis et al., J Cereb Blood Flow Metab 2002 (Brain Ischemia) : We demonstrate that in astrocytes activation of an adhesion molecule ICAM-1 by TNF-alpha is regulated through association of the phosphorylated p65 subunit of NF-kappaB with an adapter protein, p300, and that in preconditioned cells p65 remains unphosphorylated and ICAM-1 transcription is inhibited
Xie et al., Cell Microbiol 2008 (Otitis Media with Effusion) : ICAM-1 upregulation on human monocytes by the LOS required surface CD14, TLR4, NF-kappaB p65 and c-Jun N-terminal kinase (JNK) activity
Fazal et al., J Biol Chem 2009 : The effect of cofilin-1 depletion on NF-kappaB activity and ICAM-1 expression occurred downstream of IkappaBalpha degradation and was a result of impaired RelA/p65 nuclear translocation and consequently, RelA/p65 binding to DNA
Ledebur et al., J Biol Chem 1995 : Overexpression of p65 , but not p50, transactivated the ICAM-1 promoter in a kappa B site dependent manner in HUVECs
Jahnke et al., FEBS Lett 1994 (Melanoma) : Synergistic activation of intercellular adhesion molecule 1 ( ICAM-1 ) by TNF-alpha and IFN-gamma is mediated by p65/p50 and p65/c-Rel and interferon-responsive factor Stat1 alpha ( p91 ) that can be activated by both IFN-gamma and IFN-alpha
Soares et al., J Immunol 1998 : We report here that adenovirus mediated expression of a dominant negative C-terminal truncation mutant of p65/RelA ( p65RHD ) inhibits the induction of proinflammatory genes, such as E-selectin, ICAM-1 , VCAM-1, IL-8, and inducible nitric oxide synthase, in EC as efficiently as does I kappaB alpha ... We report here that adenovirus mediated expression of a dominant negative C-terminal truncation mutant of p65/RelA ( p65RHD ) inhibits the induction of proinflammatory genes, such as E-selectin, ICAM-1 , VCAM-1, IL-8, and inducible nitric oxide synthase, in EC as efficiently as does I kappaB alpha
Lee et al., Glia 1999 : These data collectively suggest that in human astrocytes, the p65 homodimer is responsible for ICAM-1 upregulation upon TNF-alpha or IL-1beta stimulation, and that IFN-gamma enhancement of ICAM-1 involves activation of STAT-1alpha homodimers
Lee et al., J Neuroimmunol 1998 : p50 overexpression had no effect on the basal levels of ICAM-1 transcription, but inhibited, in a dose dependent manner, p65 mediated transcription