Gene interactions and pathways from curated databases and text-mining

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IL6 — RENBP

Text-mined interactions from Literome

Morcos et al., Diabetes 2002 (Diabetes Mellitus, Type 2...) : The AGE- and CML dependent activation of NF-kappaBp65 and NF-kappaB dependent IL-6 expression could be inhibited using the soluble form of the receptor for AGEs (RAGE) ( soluble RAGE [ sRAGE ] ), RAGE-specific antibody, or the antioxidant thioctic acid
Sayed et al., Phytother Res 2007 : A significant reduction of AGE induced NF-kappaB-activation and Il-6 expression was observed
Liu et al., FEBS J 2009 : Pharmacological inhibitions of each individual signaling pathway, including p38, extracellular signal regulated kinase 1/2, Jun N-terminal kinase and nuclear factor-kappaB, revealed that activation of all of these four pathways is necessary for the effective induction of interleukin-6 , interleukin-8 and monochemoattractant protein-1 by both AGE-HSA and lipopolysaccharide
Rasheed et al., Rheumatology (Oxford) 2011 (Osteoarthritis) : AGE-BSA induced the expression of IL-6 and IL-8 in OA chondrocytes, which was inhibited by pre-treatment with soluble RAGE ( sRAGE ) or RAGE knockdown by siRNAs ... Treatment with SB202190 ( p38-MAPK inhibitor ) or PD98059 ( ERK inhibitor ) inhibited AGE-BSA induced IL-6 and IL-8 expression ... However, SP600125 ( JNK inhibitor ) had no effect on AGE-BSA induced IL-6 expression but inhibited the expression of IL-8 ... Treatment with NF-?B inhibitors suppressed AGE-BSA induced IL-6 and IL-8 expression ... A novel finding of our studies is that in OA chondrocytes, AGE-BSA induced expression of IL-6 , but not of IL-8, was independent of the JNK pathway ... These results demonstrate that AGE-BSA induced expression of IL-6 and IL-8 via RAGE is mediated through different MAPK signalling pathways in OA and possibly in other degenerative diseases
Cheng et al., International journal of biological sciences 2013 : TLR4 siRNA showed stronger inhibition on AGE-LDL induced IL-6 and IL-8 production than that of TLR2 siRNA ... Silencing MyD88, but not TRIF, inhibited AGE-LDL induced IL-6 and IL-8 production ... Conclusion : AGE-LDL induced IL-6 and IL-8 production via TLR2/4-MyD88 dependent pathway in tubular epithelial cells
Miki et al., Biochem Biophys Res Commun 1993 (Adenocarcinoma, Clear Cell...) : AGE-BSA showed tendency to induce in vitro cell growth of RCC cells and promoted the production of interleukin-6 (IL-6) , an in vitro autocrine growth factor