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FOS — IL3
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Seppänen et al., Oncol Res 1998
(Adenocarcinoma...) :
In the present study, we have investigated the
effects of interferons-alpha (IFN-alpha) and -gamma ( IFN-gamma ),
interleukin-10 (IL-10) and -13 ( IL-13 ), transforming growth factor-beta1 ( TGF-beta1 ), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and tumor necrosis factor-alpha (TNF-alpha) on cell proliferation and induction of transcription factors
AP-1 and NF-kappaB in UM-EC-3 human endometrial adenocarcinoma cells and UT-OC-5 ovarian carcinoma cells in vitro
Jaster et al., Biochim Biophys Acta 1999
:
Gel shift assays indicated that
IL-3 activates the binding of an AP-1 complex containing JunD to the
AP-1 sites and the binding of another protein complex to the Ets motif
Jaster et al., Cell Signal 1999
:
This hypothesis was supported by the observation that IFN-alpha, even though it had no effect on the transcription of the c-fos gene, efficiently suppressed the
IL-3 dependent expression of the
c-Fos protein
Liacini et al., Matrix Biol 2002
(Osteoarthritis, Hip) :
Inhibition of
interleukin-1 stimulated MAP kinases,
activating protein-1 (AP-1) and nuclear factor kappa B (NF-kappa B) transcription factors down-regulates matrix metalloproteinase gene expression in articular chondrocytes
Khapli et al., J Immunol 2003
:
RT-PCR analysis revealed that
IL-3 down-regulated
c-Fos transcription
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating Toll-like receptor ( TLR )
-interleukin 1 receptor (IL-1R) signaling and subsequent
activation of NF-kappaB and
AP-1 , transcriptional activators of innate immunity
Yogesha et al., J Immunol 2009
(Arthritis, Experimental...) :
We found that
IL-3 prevented TNF-alpha induced c-fos nuclear translocation and
AP-1 DNA binding activity
Gupta et al., J Immunol 2010
(Bone Resorption) :
To investigate the mechanism of IL-3 action, we analyzed the
effect of
IL-3 on the receptor activator of NF-kappaB and c-Fms receptors and
c-Fos , PU.1, NFAT cytoplasmic 1, and RelB transcription factors essential for osteoclastogenesis
Oh et al., J Cell Physiol 2012
:
IL-3 inhibited the expression of
c-Fos and NFATc1 in BMMs treated with RANKL
Chaikin et al., J Biol Chem 1994
:
While c-Jun 's induction by IL-3 is totally dependent on PKC,
c-Fos induction by
IL-3 is only attenuated by PKC depletion ...
AP-1 binding activity was also
induced by
IL-3 but this induction was PKC independent
Sung et al., J Biol Chem 1993
:
Stimulation of
interleukin-1 gene transcription may be
caused by the stimulation of transcription factor activities, including those of
AP-1 , by these protein phosphatase inhibitors
Park et al., J Biol Chem 1993
:
Using transfection and reporter gene assays specifically designed for primary T lymphocytes in conjunction with gel retardation assays, Western blot analyses and UV cross linking studies, we found that c-Jun,
c-Fos , and octamer binding proteins
play a major role in transcriptional activation of the
IL3 gene via their interaction with two specific regions contained within the IL3 5'-flanking sequence
Swiergiel et al., Brain Res Bull 1996
:
The role of cerebral noradrenergic systems in the
Fos response to
interleukin-1
Chang et al., Brain Res 1996
:
FOS expression
induced by
interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine