◀ Back to JUN

IL24 — 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
Madireddi et al., J Cell Physiol 2000 (Melanoma) : Employing a heterologous mda-7 luciferase gene reporter system, we demonstrate that ectopic expression of either AP-1/cJun or C/EBP can significantly enhance expression of the mda-7 promoter in melanoma cells
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
Kawabe et al., Mol Ther 2002 (Carcinoma, Non-Small-Cell Lung...) : Further analysis indicated that phosphorylated c-Jun expression was increased by Ad-mda7 in both A549 and H1299 cells, but not in CCD-16 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
Yacoub et al., Mol Pharmacol 2010 (Ovarian Neoplasms) : In a PERK dependent fashion, MDA-7/IL-24 reduced ERK1/2 and AKT phosphorylation and activated c-Jun NH ( 2 ) -terminal kinase ( JNK ) 1/2 and p38 mitogen activated protein kinase ( MAPK )
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
Huo et al., Oncol Rep 2013 : The results showed that MDA-7/IL-24 overexpression decreased the expression of CD44, ICAM-1, MMP-2/-9, CyclinB, Twist, survivin, TGF-ß and p-Akt, transcriptional activity of NF-?B, and increased the expression of E-cadherin and p-ERK and transcriptional activity of AP-1 in HepG2 and BEL-7402 cells
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