Gene interactions and pathways from curated databases and text-mining

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FOS — RNF19A

Text-mined interactions from Literome

Silvers et al., Neoplasia (New York, N.Y.) 2003 (Skin Neoplasms) : These results demonstrated that activation of both JNK and p38 play critical role in UVA mediated AP-1 transactivation and c-Fos expression in these human keratinocyte cells
Chun et al., Carcinogenesis 2004 : In order to clarify the roles of p38 and ERK in TPA induced AP-1 activation, we utilized the pharmacologic inhibitors of these enzymes
Gao et al., Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 2006 : ERK and JNK, but not p38 , mediated benzo ( a ) pyrene induced cell cycle changes by AP-1 transactivation in HELF
Tirumurugaan et al., Am J Physiol Lung Cell Mol Physiol 2007 (MAP Kinase Signaling System) : EMSAs confirmed the role of p38 and JNK in mediating NF-kappaB and AP-1 activation
Humar et al., Int J Biochem Cell Biol 2007 : Moreover, DNA binding activity of c-Fos , FosB, and JunB were also dependent on the p38 protein kinase activity, whereas JunD, Fra-1 and Fra-2 were not affected
Irarrazabal et al., J Biol Chem 2008 : Thus, AP-1 is part of the TonEBP/OREBP enhanceosome, and its role in high NaCl induced activation of TonEBP/OREBP may require p38 activity
Yang et al., Atherosclerosis 2010 : N-acetylcysteine, SP600125 ( JNK inhibitor ) and SB203580 ( p38 MAPK inhibitor ) attenuated TNF-alpha induced DNA binding activities of both AP-1 and NF-kappaB
Son et al., Oncol Rep 2010 (Melanoma, Experimental) : Ethanol extract of Lycoris radiata induces cell death in B16F10 melanoma via p38 mediated AP-1 activation
Butoi et al., Biochim Biophys Acta 2011 : Monocyte-SMC interaction induced the phosphorylation of p38MAPK and activation of AP-1 transcription factor
Tan et al., J Cell Physiol 2012 : Moreover, CCN3 induced c-Jun translocation into the nucleus, and the binding of c-Jun to the AP-1 element on the BMP-4 promoter were both inhibited by specific inhibitors of the ILK, p38 , and JNK cascades
Saadane et al., Journal of inflammation (London, England) 2011 : This was associated with enhanced phosphorylation of p38 , ERK1/2 and JNK and increased activation of AP-1