Gene interactions and pathways from curated databases and text-mining

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HMGB1 — JUN

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Henderson et al., J Virol 2000 : HMG I binding to this composite site inhibits the binding of recombinant AP-1
Hommura et al., Mol Cancer Res 2004 : HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of c-Jun expression, and gel mobility shift assays demonstrate that induced c-Jun binds to an AP-1 consensus site at position -1,091 in the HMG-I/Y promoter
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
Nadatani et al., Am J Pathol 2012 (Peptic Ulcer) : In wild-type mice, recombinant human HMGB1 aggravated indomethacin induced small intestinal damage ; enhanced the mRNA expression levels of tumor necrosis factor a (TNF-a), monocyte chemotactic protein 1, and KC ; activated nuclear factor kappa B ; and stimulated phosphorylation of the mitogen activated protein kinases p38, extracellular signal regulated kinase ( ERK ), and c-Jun N-terminal kinase (JNK)