◀ Back to IL6
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