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IL13 — JUN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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
Masuda et al., J Immunol 2002
(MAP Kinase Signaling System) :
In contrast, inhibition of
c-Jun N-terminal kinase activation significantly
suppressed both IL-10 and
IL-13 expression at both mRNA and protein levels
Hirasawa et al., FEBS Lett 2003
:
These findings suggest that the inhibition of antigen induced
IL-13 production by dexamethasone is
due to the GR-mediated inhibition of
c-Jun phosphorylation induced by JNK
Li et al., Zhonghua Shao Shang Za Zhi 2004
(Acute Lung Injury) :
The pulmonary
AP-1 activity
increased with the enhanced expression of
IL-13 , which was related to the development of SIRS-ALI
Masuda et al., J Immunol 2004
:
The interaction between GATA proteins and
activator protein-1 promotes the transcription of
IL-13 in mast cells ... The results of the present study have shown that direct interaction between
AP-1 and GATA proteins
plays an important role in
IL-13 transcription in mast cells
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
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
Fujisawa et al., Cancer Res 2009
(Neoplasm Invasiveness...) :
Mechanistically,
IL-13 activated extracellular signal regulated kinase 1/2 and
activator protein-1 nuclear factors in IL-13Ralpha2 positive pancreatic cancer cell lines but not in IL-13Ralpha2 negative cell lines
Shimamura et al., Clin Cancer Res 2010
(Adenocarcinoma...) :
c-Jun and c-Fos of the AP-1 family of nuclear factors were
activated by
IL-13 only in IL-13Ralpha2 positive cells
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 ]
Fujisawa et al., Int J Cancer 2012
(Neoplasm Invasiveness...) :
Mechanistically,
IL-13 enhanced ERK1/2,
AP-1 and MMP activities only in IL-13Ra2 positive cells but not in IL-13Ra2 negative cells
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
Manna et al., J Immunol 1998
:
TNF induced activation of another nuclear transcription factor,
AP-1 , was
suppressed by
IL-13