Gene interactions and pathways from curated databases and text-mining

◀ Back to IL6

IL6 — IRS1

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: IRS1 → IL6 (decreases)
    Evidence: IL-6 in vitro reduces insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation, as well as IRS-1-associated phosphatidylinositol (PI) 3-kinase activity (55),
  • OpenBEL Selventa BEL large corpus: IRS1 → IL6 (decreases)
    Evidence: Furthermore, IL-6 directly impairs insulin signalling in primary mouse hepatocytes and 3T3-L1 adipocytes with decreased activation of IRS-1 and PI 3-kinase, as well as impaired insulin-induced glycogenesis in liver cells [38, 39].

Text-mined interactions from Literome

Kim et al., J Biol Chem 2005 (Inflammation) : In addition, using a phospho-specific antibody against IRS-1 phosphorylated at Ser ( 24 ), we found that interleukin-1 or TNF-alpha treatment of Fao cells stimulated increased phosphorylation of endogenous IRS-1 at Ser ( 24 )
Weigert et al., J Biol Chem 2006 : Moreover, IL-6 induced a rapid and transient phosphorylation of Ser-318 of IRS-1 in muscle cells and in muscle tissue, but not in the liver of IL-6 treated mice, probably via the IL-6 induced co-recruitment of protein kinase C-delta
Andreozzi et al., Mol Cell Biol 2007 : We observed that IL-6 increased IRS-1 phosphorylation at Ser ( 312 ) and Ser ( 616 ) ; these effects were paralleled by increased Jun N-terminal protein kinase (JNK) and extracellular signal regulated kinase 1/2 ( ERK1/2 ) phosphorylation and reversed by JNK and ERK1/2 inhibition
Tang et al., J Immunol 2007 : Leptin induced IL-6 production is mediated by leptin receptor, insulin receptor substrate-1 , phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 pathway in microglia
Huppertz et al., Diabetologia 1996 : The effects of insulin, insulin-like growth factor (IGF)-I, platelet derived growth factor ( PDGF ), interleukin (IL)-6 and interferon-gamma on 2-deoxyglucose uptake and insulin receptor substrate (IRS)-1 phosphorylation were compared in 3T3-L1 cells at confluence and after differentiation to the adipocyte-like phenotype