◀ Back to IL10

IL10 — 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
Raychaudhuri et al., Cytokine 2000 : AP-1 was not affected by IL-10
Gollnick et al., Photochem Photobiol 2001 : However, in contrast to PDT, UVB induced activation of the IL-10 promoter is not AP-1 dependent and did not increase IL-10 mRNA stability
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
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
Mohamed et al., Bone 2007 : IL-10 potently reduced the RANKL induced expression of NFATc1, c-Jun and c-Fos, which are known to be essential for osteoclastogenesis, in time- and dose dependent manners
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
Wallet et al., Cell Immunol 2010 (Inflammation) : IFNgamma primed, HMW-HA activated macrophages produced elevated levels of TNF and secreted the TH1 cytokine IL-12p70, while IFNgamma suppressed HMW-HA induced secretion of the regulatory cytokine IL-10 and activation of the transcription factor c-Jun
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 ] ... To study the expression of intercellular cell adhesion molecule-1 ( ICAM-1 ), Interleukin-10 (IL-10) and the activation of transcription factor activator protein-1 (AP-1) in a rabbit model of ventilator induced lung injury ( VILI ) and therefore to explore their possible role in VILI
Guindi et al., Cell Immunol 2012 (MAP Kinase Signaling System) : ERK1/2 and AP-1 were involved in IL-10 production in GM/DCs but not in their resistance to maturation
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
Li et al., Nature 2012 : Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in T ( H ) 17 cells and potently regulated by IL-21
Yin et al., Eur J Cell Biol 2013 : The results demonstrated that IL-10 significantly blocked the phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) and apoptosis induced by oxLDL
Hurme et al., Immunol Lett 1994 : Effect of interleukin-10 on NF-kB and AP-1 activities in interleukin-2 dependent CD8 T lymphoblasts
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
Finnegan et al., J Immunol 1996 (Lymphoma, Large B-Cell, Diffuse) : In combination with TNF-alpha, IL-10 stimulated activating protein-1 (AP-1) and nuclear factor (NF)-kappa B binding activities and cooperated to increase HIV-1 steady-state mRNA levels and enhance long terminal repeat directed transcription through activation of the NF-kappa B binding sites, suggesting the IL-10 effect occurs at least in part at the transcriptional level
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 ... However, for IL-4 this was accompanied with a reduction of AP-1 and NF-IL6 binding activity whereas IL-10 only inhibited 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