Gene interactions and pathways from curated databases and text-mining

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FOS — NOS2

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Hsu et al., J Immunol 2001 : In conclusion, we suggest that ceramide inhibition of LPS mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1 , which might result from ceramide 's inhibition of LPS stimulated IkappaB kinase, p38 mitogen activated protein kinase, and protein kinase C
Kizaki et al., Biochem Biophys Res Commun 2001 : Negative regulation of LPS stimulated expression of inducible nitric oxide synthase by AP-1 in macrophage cell line J774A.1
Mendes et al., Nitric Oxide 2002 : In conclusion, this study shows that ( 1 ) PTK are part of the signaling pathway that leads to IL-1 induced NF-kappaB activation and iNOS expression ; ( 2 ) the p38MAPK cascade is required for IL-1 induced iNOS expression ; ( 3 ) the p42/44MAPK and AP-1 are not involved in IL-1 induced iNOS expression ; and ( 4 ) NF-kappaB and the p38MAPK lie on two distinct pathways that seem to be independently required for IL-1 induced iNOS expression
Cho et al., Nitric Oxide 2002 (MAP Kinase Signaling System) : These results demonstrated that bovine type I collagen induces iNOS in serum stimulated murine macrophages through JunB/AP-1 and NF-kappa B activation and that activation of ERK1/2 plays an essential role in JunB/AP-1 activation
Lee et al., Br J Pharmacol 2003 : The effects of sauchinone on the inducible nitric oxide synthase (iNOS) , tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase 2 (COX-2) gene expression and on the activation of transcription factors, nuclear factor-kappaB (NF-kappaB), CCAAT/enhancer binding protein (C/EBP), activator protein-1 (AP-1) and cAMP-response element binding protein ( CREB ) were determined in Raw264.7 cells as part of the studies on its anti-inflammatory effects
Lee et al., Life Sci 2003 : The regulation of inducible nitric oxide synthase gene expression induced by lipopolysaccharide and tumor necrosis factor-alpha in C6 cells : involvement of AP-1 and NFkappaB ... The roles of AP-1 and NFkappaB in the regulation of inducible nitric oxide synthase (iNOS) mRNA expression induced by the combination of lipopolysaccharide and tumor necrosis factor-alpha ( LT ) in C6 cells were examined in the present study
Okada et al., Int Immunol 2003 : Since introduction of a double mutation into the two AP-1 binding sites in the iNOS promoter region reduced the promoter activity to 25 % of the authentic one in activated RAW264 cells, the induced c-Fos/AP-1 may promote iNOS expression in activated macrophages ... Since introduction of a double mutation into the two AP-1 binding sites in the iNOS promoter region reduced the promoter activity to 25 % of the authentic one in activated RAW264 cells, the induced c-Fos/AP-1 may promote iNOS expression in activated macrophages
Mendes et al., Cell Biol Toxicol 2003 (Inflammation) : Since we observed that AP-1 is not required for iNOS expression in chondrocytes, we also investigated whether it is a repressor of this gene
Cho et al., Biochim Biophys Acta 2005 : BIC also induces nitric oxide synthase in macrophages through JunB/AP-1 and NF-kappaB activation
Jang et al., Biochem Biophys Res Commun 2005 : AP-1 mediates beta-amyloid induced iNOS expression in PC12 cells via the ERK2 and p38 MAPK signaling pathways ... The above findings suggest that A beta induces iNOS expression in PC12 cells through activation of AP-1 which is regulated by upstream kinases, such as ERK and p38 MAPK
Oh et al., J Pharm Pharmacol 2005 : The effects of these glycosides on activator protein-1 (AP-1) mediated inducible nitric oxide synthase (iNOS) gene expression in the Raw264.7 macrophage cell line have been studied
Choi et al., J Biomed Sci 2005 : Chrysoeriol potently inhibits the induction of nitric oxide synthase by blocking AP-1 activation
Shimizu et al., J Hepatol 2007 (Hemorrhage...) : Although both PPT and DPN decreased hepatic injury following trauma-hemorrhage, ER-alpha agonist PPT appears to be more effective in downregulating NF-kappaB and AP-1 activity, and iNOS induction
Lee et al., J Biomed Sci 2008 (Colitis...) : In addition, consumption of UDN glycoprotein attenuated the activities of proliferating cell nuclear antigen ( PCNA ), inducible nitric oxide synthase (iNOS) , and cyclooxygenase-2 (COX-2), and inhibited the DNA binding activities of nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) in the mice colonic tissue
Qian et al., Mol Cell Endocrinol 2007 : Transcriptional regulation of endothelial nitric oxide synthase expression in uterine artery endothelial cells by c-Jun/AP-1
Hasselblatt et al., Proc Natl Acad Sci U S A 2007 (Drug-Induced Liver Injury...) : Hepatocyte survival in acute hepatitis is due to c-Jun/AP-1 dependent expression of inducible nitric oxide synthase
Chen et al., Eur J Pharmacol 2008 (MAP Kinase Signaling System) : We suggested that interfering with JNK mediated c-Jun phosphorylation and thus blocking AP-1 activation might contribute to the suppression effects of 8-prenylkaempferol on iNOS
Chambellan et al., Nitric Oxide 2009 : Pivotal role of c-Fos in nitric oxide synthase 2 expression in airway epithelial cells
Wang et al., J Cell Biochem 2009 (Orthostatic Intolerance) : A key role for AP-1 , but not NF-kappaB in the regulation of iNOS was shown
Lee et al., J Ethnopharmacol 2009 : Moreover, inhibition of LPS induced iNOS expression by BV was dependent on transcriptional activities of AP-1/NF-kappaB through MEK/ERK pathway
Cho et al., Dig Dis Sci 2010 (Adenocarcinoma...) : Involvement of Ras and AP-1 in Helicobacter pylori induced expression of COX-2 and iNOS in gastric epithelial AGS cells ... We investigated whether H. pylori in a Korean isolate ( HP99 ), a cagA ( + ), vacA ( + ) strain, induces the expression of c-Fos and c-Jun for AP-1 activation to induce COX-2 and iNOS and whether HP99 induced expressions of COX-2 and iNOS are mediated by Ras and AP-1 , determined by the expressions of c-Fos and c-Jun, in gastric epithelial AGS cells, using transfection with mutant genes for Ras ( ras N-17 ) and c-Jun ( TAM-67 )
Do et al., J Nutr Biochem 2010 (Brain Neoplasms...) : Suppression of iNOS expression by fucoidan is mediated by regulation of p38 MAPK, JAK/STAT, AP-1 and IRF-1, and depends on up-regulation of scavenger receptor B1 expression in TNF-alpha- and IFN-gamma stimulated C6 glioma cells
Ban et al., Mol Cell Biochem 2011 (Inflammation...) : Lastly, the specific iNOS inhibitor, 1400W, had no effect on either AP-1 or c-Jun
Ratajczak-Wrona et al., J Immunotoxicol 2013 (MAP Kinase Signaling System) : Role of AP-1 family proteins in regulation of inducible nitric oxide synthase (iNOS) in human neutrophils
Tsai et al., J Dermatol Sci 2013 (Gram-Positive Bacterial Infections...) : ROS dependent stimulation of ERK, JNK, NF-?B, and AP-1 activation contributes to P. acnes induced iNOS/NO and COX-2/PGE ( 2 ) in macrophages, and chemicals such as hispolon possessing ability to block iNOS/NO and COX-2/PGE ( 2 ) production reserve potential to be further developed for treatment of the early phase of inflammation elicited by P. acnes
Kwon et al., Endocrinology 1996 : Interleukin 1-induced Fos and Jun do not regulate inducible nitric oxide synthase in rat islets of Langerhans and RINm5F cells ... Temporal correlation of Fos and Jun expression and iNOS gene induction suggested that Fos and Jun might regulate iNOS gene transcription by rodent pancreatic beta-cells
Zhu et al., Neuroscience 1997 : Since our previous results showed that glutamate blockade, but not nitric oxide synthase inhibition, suppressed angiotensin II-induced c-Fos , the experiments reported here further suggest that nitric oxide release is not an essential requirement for the expression of c-fos elicited by angiotensin II
Marks-Konczalik et al., J Biol Chem 1998 : The involvement of AP-1 and NF-kappaB transcription factors in cytokine mediated induction of human inducible nitric oxide synthase ( hiNOS ) promoter activity was examined