Gene interactions and pathways from curated databases and text-mining

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FOS — IL13

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
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 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
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
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
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
Manna et al., J Immunol 1998 : TNF induced activation of another nuclear transcription factor, AP-1 , was suppressed by IL-13