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IL3 — JUN
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
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
Wheadon et al., Blood 2003
:
Induction of TEL/PDGFbetaR expression led to increased cell survival following
IL-3 withdrawal and constitutive
activation of protein kinase B (PKB), signal transducer and activator of transcription 5 ( STAT5 ), extracellular signal regulated kinases 1/2 ( ERK1/2 ),
Jun N-terminal kinases 1/2 (JNK1/2) , and p38 mitogen activated protein kinase ( MAPK ) pathways
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
Shen et al., Curr Eye Res 2009
:
Under high glucose conditions,
interleukin-1beta significantly
increased expression of
c-Jun and decreased the expression of glutamine synthetase
Zhang et al., Zhonghua Jie He He Hu Xi Za Zhi 2010
(Ventilator-Induced Lung Injury) :
[ Expression of intercellular cell adhesion molecule-1,
interleukin-10 and the
activation of
activator protein-1 in ventilator induced lung injury in rabbits ]
Byun et al., Biochem Biophys Res Commun 2012
(Inflammation) :
In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a,
interleukin [ IL]-1ß, and IL-6 ) and
activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38,
c-Jun N-terminal kinase (JNK) , and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Chaikin et al., J Biol Chem 1994
:
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
Schwenger et al., Proc Natl Acad Sci U S A 1997
:
c-Jun N-terminal kinase activation
induced by
interleukin 1 or epidermal growth factor was less strongly inhibited by NaSal
Sansbury et al., Carcinogenesis 1997
(Thymoma) :
Phorbol ester induced morphological changes, ERK activation, calcium dependent
activation of the
c-Jun N-terminal kinase (JNK) ,
interleukin-2 synthesis, and growth inhibition in sensitive but not resistant cells