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IL4 — JUN
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Zhang et al., J Immunol 1999
:
T cell proliferation and production of IL-2,
IL-4 , and IFN-gamma
induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the
c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580
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
Rebollo et al., Mol Cell Biol 2000
:
Retardation gels showed that
IL-4 specifically
induces AP1 and AP1-like binding activity and that mutation of these binding sites abolishes the IL-4 induced Bcl-3 promoter activity, suggesting that these transcription factors are important in Bcl-3 promoter transactivation ...
IL-4 deprivation
induces downregulation of
Jun expression and upregulation of Fos expression, both of which are proteins involved in the formation of AP1 and AP1-like transcription factors
Shen et al., J Immunol 2001
:
By contrast, C/EBP beta, which trans-activates the human GL epsilon promoter,
inhibits IL-4 induction of the mouse promoter, probably by attenuating the synergistic interaction between
AP-1 and Stat6
Vereshchagina et al., J Immunol 2001
:
Moreover,
IL-4 induced binding of CREB and
AP-1 to the upstream promoter elements and resulted in increased CR2 surface protein expression
Yamazaki et al., J Dermatol Sci 2002
(Dermatitis, Atopic...) :
Overactivation of
IL-4 induced
activator protein-1 in atopic dermatitis ... Together, our present study indicates that
AP-1 is over
activated by
IL-4 in PBMC of the atopic patients with the higher IgE level, thereby implying that IL-4 induced over-activation of AP-1 might be one of pathogenic factors in atopic dermatitis
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
Maeda et al., J Invest Dermatol 2003
:
Electrophoretic mobility shift assays using [ 32P ] -labeled synthetic oligonucleotides encoding the consensus binding motif of activator protein-1 demonstrated that
interleukin-4 induced binding of
activator protein-1 composed of JunB was interfered by terfenadine
Lgssiar et al., Experimental biology and medicine (Maywood, N.J.) 2004
(Diabetes Mellitus, Experimental) :
Interleukin-11 prevented diabetes without affecting insulitis ; attenuated TNF-alpha and IFN-gamma response ; and stimulated
IL-4 production and
inhibited activation of IKK-alpha, NF-kappaB, and
AP-1
Nolan et al., J Biol Chem 2005
(Inflammation) :
The evidence indicates that
IL-4 modulates expression of IL-1beta mRNA and protein and that it
attenuates IL-1beta induced impairment of LTP and phosphorylation of JNK and
c-Jun
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
El Mabrouk et al., J Cell Biochem 2008
:
IL-4 did not
affect OSM stimulated phosphorylation of extracellular signal regulated kinases ( ERKs ), protein 38 (p38),
c-Jun N-terminal kinase (JNK) and Stat1
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
Chambers et al., Exp Cell Res 2013
(Periodontitis) :
IL-4 inhibition of IL-1 induced Matrix Metalloproteinase-3 (MMP-3) expression in human fibroblasts
involves decreased
AP-1 activation via negative crosstalk involving of Jun N-terminal Kinase (JNK)
Rooney et al., Immunity 1995
:
Coordinate and cooperative
roles for NF-AT and
AP-1 in the regulation of the murine
IL-4 gene
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
Dokter et al., Blood 1993
:
Interleukin-4 inhibits the lipopolysaccharide induced expression of c-jun and c-fos messenger RNA and
activator protein-1 binding activity in human monocytes ... Finally, using electrophoretic mobility shift assays, evidence was obtained that
IL-4 inhibits LPS induced expression of
AP-1 protein
Dokter et al., Leukemia 1996
:
In electrophoretic mobility shift assays ( EMSAs ) we showed that IL-10 and
IL-4 inhibited LPS induced
AP-1 binding activity
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