Gene interactions and pathways from curated databases and text-mining

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HMGB1 — MAPK3

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

Kawahara et al., Cardiovasc Pathol 2008 (Inflammation) : C-reactive protein induces high-mobility group box-1 protein release through activation of p38MAPK in macrophage RAW264.7 cells
Yuk et al., Antioxid Redox Signal 2009 (Inflammation) : In addition, HMGB1 induced activation of p38 and c-Jun N-terminal kinase (JNK), but not extracellular signal regulated kinase 1/2 , was strongly abrogated by the overexpression of APE1 ... In addition, HMGB1 induced activation of p38 and c-Jun N-terminal kinase (JNK), but not extracellular signal regulated kinase 1/2 , was strongly abrogated by the overexpression of APE1
Kawahara et al., Int J Mol Med 2008 (Atherosclerosis...) : The p38MAPK inhibitor SB203580 and the 5-HT1B antagonist GR55526 markedly inhibited HMGB1 release from 5-HT stimulated HUVECs ... HMGB1 induced the activation of p38MAPK , ERK1/2 and Akt
Oyama et al., Lab Invest 2010 (Granuloma...) : HMGB1 also induced MCP-1 secretion through mitogen activated protein kinase ( MAPK ) and phosphoinositide-3-kinase (PI3K) pathways in rat renal tubular epithelial cells in vitro
Xu et al., J Biol Chem 2011 (MAP Kinase Signaling System) : HMGB1 induced Erk1/2 and p38 phosphorylation is abolished when endothelial heparan sulfate is removed or blocked pharmacologically, resulting in decreased HMGB1 induced endothelial sprouting
Zhu et al., Int J Mol Med 2013 : However, extracellular HMGB1 , which is actively or passively released under different conditions, can act as a key inflammatory mediator through MyD88/mitogen activated protein kinase signaling by binding to its receptors including the receptor for advanced glycation end products or Toll-like receptors
Lu et al., J Interferon Cytokine Res 2013 : Interestingly, overexpression of Mfn-2 had no marked effect on HMGB1 mediated activation of MAPK , but could attenuate the suppressive effect of HMGB1 on the activity of NFAT