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HSF1 — IL6

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: HSF1 → IL6 (increases, IL6 Activity)
  Evidence: IL6, which is also considered a proinflammatory mediator in synovitis, when added to fibroblast like synoviocytes at a concentration of 10ng/ml, induced HSF1 activation but weaker upregulation of hsp70.

Text-mined interactions from Literome

Tang et al., Biochem Biophys Res Commun 2001 : However, in Ku-deficient cells, NF-IL6 was still able to displace HSF1 from heat shock element ( HSE ) and repressed HSF1 activation
Takii et al., J Immunol 2010 (Fever) : Heat shock transcription factor 1 inhibits expression of IL-6 through activating transcription factor 3 ... Heat shock transcription factor 1 (HSF1) activated by heat shock induced the expression of activating transcription factor (ATF) 3, a negative regulator of IL-6, and ATF3 was necessary for heat mediated suppression of IL-6 , indicating a fever mediated feedback loop consisting of HSF1 and ATF3
Ambade et al., Hepatology 2012 (Disease Models, Animal...) : Chromatin immunoprecipitation assays showed that 17-DMAG enhanced HSF1 binding to the TNFa promoter, but not the IL-6 promoter, suggesting HSF1 mediated direct inhibition of TNFa, but not IL-6 ... We show that HSF1 indirectly regulates IL-6 by the induction of another transcription factor, activating transcription factor 3 ... Inhibition of HSF1 , using small interfering RNA, prevented 17-DMAG mediated down-regulation of NF?B binding activity, TNFa, and IL-6 induction, supporting a repressive role for HSF1 on proinflammatory cytokine genes during hsp90 inhibition
Welc et al., Am J Physiol Cell Physiol 2013 (Fever) : Overexpression of a constitutively active HSF-1 construct increased basal ( 37°C ) promoter activity, whereas overexpression of a dominant negative HSF-1 reduced IL-6 promoter activity during basal and hyperthermia conditions ... These studies demonstrate that IL-6 regulation in hyperthermia is directly controlled by HSF-1 and AP-1 signaling and that the IL-6 response in C2C12 myotubes is sensitive to categories of protein stress that reflect accumulation of damaged or unfolded proteins