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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