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HMGB1 — NFKB1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Pullerits et al., Arthritis Rheum 2003
(Arthritis, Experimental...) :
In addition, spleen cells were cultured in the
presence of
HMGB-1 , and
nuclear factor kappaB (NF-kappaB) activation was detected by electrophoretic mobility shift assay
Park et al., J Biol Chem 2004
:
Transfections with dominant negative constructs demonstrated that TLR 2 and TLR 4 were both involved in
HMGB1 induced activation of
NF-kappaB
Dumitriu et al., J Immunol 2005
:
HMGB1/RAGE interaction
results in downstream activation of MAPKs and
NF-kappaB
Völp et al., Gut 2006
(Colonic Neoplasms) :
HMGB1 increased
NFkappaB activity and led to co-overexpression of the antiapoptotic NFkappaB target gene product c-IAP2 in vitro
Maeda et al., Biochem Biophys Res Commun 2007
(Colitis...) :
In macrophages,
HMGB1 induces several proinflammatory cytokines, such as IL-6, which are
regulated by
NF-kappaB activation ... In macrophages,
HMGB1 induces several proinflammatory cytokines, such as IL-6, which are
regulated by
NF-kappaB activation
van Beijnum et al., Angiogenesis 2008
(Neovascularization, Pathologic) :
Furthermore,
HMGB1 induced signaling can
activate NFkappaB , which can subsequently induce the expression of HMGB1 receptors
Lv et al., Thromb Haemost 2009
:
Moreover,
HMGB1 increased expression of Egr-1 and nuclear translocation of
NF-kappaB ( c-Rel/p65 ) in ECs ... Moreover,
HMGB1 increased expression of Egr-1 and nuclear translocation of
NF-kappaB ( c-Rel/p65 ) in ECs ... Taken together, our data suggest that
HMGB1 induces TF expression in vascular endothelial cells via cell surface receptors ( TLR4, TLR2, and RAGE ), and through activation of transcription factors (
NF-kappaB and Egr-1 )
Feng et al., Int Immunopharmacol 2013
(Diabetes Mellitus...) :
Immunofluorescence and Western blotting assays showed that CM1 could attenuate
HMGB1 induced intracellular ERK1/2 and
NF-kB activation in HUVECs