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IL5 — JUN
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
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
Heijink et al., Immunology 2002
:
This is not the case for the short-term IL-6 effect on
IL-5 secretion, where the p38 mitogen activated protein kinase dependent induction of
activator protein-1 DNA binding activity is
involved , independent of signal transducer and activator of transcription 3 phosphorylation
Wang et al., Int Immunol 2006
(MAP Kinase Signaling System) :
AP-1 ( c-Fos/c-Jun ) strongly
induced IL-5 transcription and dominant negative AP-1 constructs confirmed that AP-1 plays an important role in regulating IL-5 expression ...
AP-1/Ets1 transactivation also
stimulated IL-5 mRNA expression
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
Wang et al., Allergy 2007
(Inflammation) :
Dominant negative
AP-1 inhibited
IL-5 transcription
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
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
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