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FOS — IL7

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
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
Ming et al., Cancer Immunol Immunother 2012 (Carcinoma, Non-Small-Cell Lung...) : We found that, in lung cancer cell lines and in nude mice, Interleukin-7/Interleukin-7 receptor increased the expression of cyclin D1 and phosphorylation of c-Fos/c-Jun, induce c-Fos and c-Jun heterodimer formation, and enhanced c-Fos/c-Jun DNA binding activity to regulate cyclin D1
Ming et al., Zhonghua Bing Li Xue Za Zhi 2012 (Carcinoma, Non-Small-Cell Lung...) : IL-7/IL-7R could promote proliferation of A549 cell, increase cyclin D1 and VEGF-D expression, and enhance c-Fos/c-Jun expression and phosphorylation, resulting in formation of heterodimer ... Furthermore, IL-7/IL-7R could induce binding of c-Fos/c-Jun to cyclin D1/VEGF-D promoters and regulate their transcription
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
Swiergiel et al., Brain Res Bull 1996 : The role of cerebral noradrenergic systems in the Fos response to interleukin-1
Chang et al., Brain Res 1996 : FOS expression induced by interleukin-1 or acute morphine treatment in the rat hypothalamus is attenuated by chronic exposure to morphine
Gringhuis et al., Blood 1997 (Leukemia-Lymphoma, Adult T-Cell) : We also show that the IL-7 induced enhancement of the AP-1-DNA binding activity is not cyclosporin A-sensitive