◀ Back to IL6
IL6 — JUND
Text-mined interactions from Literome
Granger et al., Biochim Biophys Acta 2000
:
Whilst the expression of
JunD was not affected by any of the mediators, the mRNA levels of c-fos and JunB were
induced by LPS,
IL-6 , IFN-gamma, PDGF and TNF-alpha, and that of c-jun by LPS, IFN-gamma, PDGF and TNF-alpha
Smart et al., J Biol Chem 2001
(Liver Cirrhosis) :
JunD regulates transcription of the tissue inhibitor of metalloproteinases-1 and
interleukin-6 genes in activated hepatic stellate cells ... In this study, we used expression vectors for wild-type, dominant negative, and forced homodimeric ( Jun/eb1 chimeric factors ) forms of JunD and other Fos and Jun proteins to determine the
requirement for
JunD in the transcriptional regulation of the TIMP-1 and
interleukin-6 (IL-6) genes ...
IL-6 promoter activity was induced upon activation of HSCs and also
required JunD activity ; however, expression of JunD/eb1 homodimers resulted in transcriptional repression ... We conclude that
JunD activates
IL-6 gene transcription as a heterodimer and operates at an alternative DNA binding site in the promoter
Mann et al., J Biol Chem 2002
:
Overexpression of an IkappaB-alpha super-repressor or a dominant negative
JunD resulted in a strong inhibition of CD40-inducible
IL-6 promoter activity supporting a role for both transcription factors
Zerbini et al., Cancer Res 2003
(Neoplasms, Hormone-Dependent...) :
Constitutive activation of nuclear factor kappaB p50/p65 and Fra-1 and
JunD is
essential for deregulated
interleukin 6 expression in prostate cancer ... Our data demonstrate for the first time that a combined aberrant activation of NF-kappaB p50 and p65 and AP-1
JunD and Fra-1 in androgen independent prostate cancer cells
results in deregulated
IL-6 expression, suggesting a novel potential entry point for therapeutic intervention in prostate cancer
Zerbini et al., Cell cycle (Georgetown, Tex.) 2011
(Prostatic Neoplasms) :
We previously established that activation of the AP-1 family member
JunD contributes to deregulated expression of the anti-apoptotic
IL-6 gene in prostate cancer cells