Gene interactions and pathways from curated databases and text-mining

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IL6 — PTPN11

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Chauhan et al., J Biol Chem 2000 (Multiple Myeloma) : We show that IL-6 triggers selective activation of SHP2 and its association with RAFTK in Dex treated MM cells
Anderson et al., Semin Hematol 2001 (Multiple Myeloma) : Apoptosis of myeloma cells triggered by corticosteroids is mediated by related focal adhesion tyrosine kinase ( RAFTK ) ; blocking RAFTK inhibits this apoptosis inducing effect IL-6 activates SHP2 , which inhibits RAFTK activation, thereby protecting multiple myeloma cells from the apoptotic effects of corticosteroids
Hideshima et al., Oncogene 2001 (MAP Kinase Signaling System...) : We demonstrate that Dex induced apoptosis in MM.1S cells is mediated by downstream activation of caspase-9, with resultant caspase-3 cleavage ; and conversely, that IL-6 triggers activation of PI3-K and its association with SHP2 , inactivates caspase-9, and protects against Dex induced apoptosis
Sobota et al., Cell Signal 2008 : Mouse embryonic fibroblasts expressing a SIRP1alpha protein which lacks the intracellular part show enhanced SHP2 phosphorylation and ERK1/2 activation in response to IL-6 , suggesting that SIRP1alpha affects IL-6 signalling through SHP2
Wilson et al., J Virol 2008 : Furthermore, NS1 expression also inhibited TLR3 dependent production of interleukin-6 and the establishment of an antiviral state
Graf et al., Arch Biochem Biophys 2008 : CD95L induced caspase activation leads to degradation of gp130, thereby suppressing IL-6 induced phosphorylation of STAT3 ( Tyr ( 705 ) ) and of tyrosine phosphatase SHP2 ( Tyr ( 580 ) )
Chen et al., J Cell Biochem 2010 (Inflammation) : In contrast, inhibition of SHP-2 enzymatic activity ( sodium stibogluconate ) abrogated the increased ERK phosphorylation associated with integrin beta4 silencing in LPS treated EC and attenuated the increases in levels of IL-6 and IL-8 in integrin-beta4 silenced EC
Moffatt et al., J Virol 1996 : Our novel finding, IL-6 induction by NS1 , supports the possible relationship between parvovirus B19 infection and polyclonal activation of B cells in rheumatoid arthritis and indicates that NS1 protein may play a significant role in the pathogenesis of some B19 associated diseases by modulating the expression of host cellular genes
Berger et al., Blood 1997 (Multiple Myeloma) : Prior treatment of U266 cells with IFN-beta downregulated IL-6 induced tyrosine phosphorylation of gp130, Jak2, PTP1D/Syp , Shc, and Erk2, and GTP loading of p21ras ... Further analysis indicated that treatment with IFN-beta disrupted IL-6 induced binding of PTP1D/Syp to gp130 and the adaptor protein Grb2 ; IFN-beta pretreatment also interfered with IL-6 induced interaction of Shc with Grb2 and a 145-kD tyrosine phosphorylated protein
Moffatt et al., J Virol 1998 : Mutations engineered into the nucleoside triphosphate binding domain of NS1 significantly rescued cells from NS1 induced apoptosis without having any effect on NS1 induced activation of the IL-6 gene expression which is mediated by NF-kappaB ... Furthermore, using pentoxifylline, an inhibitor of NF-kappaB activation, we demonstrate that the NF-kappaB mediated IL-6 activation by NS1 is uncoupled from the apoptotic pathway
Ogata et al., Clin Cancer Res 1997 (Multiple Myeloma) : gp130 phosphorylation, gp130-to-PTP1D binding, PTP1D phosphorylation, and PTP1D-to-Grb2 binding are also induced by IL-6 in all IL-6 independent MM cell lines studied