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Modules
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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
9094TNFProteinHomo sapiens-eIncreases expressionindirectPTGS2ProteinHomo sapiens-e
These studies demonstrated that IL-1beta, TNFalpha, IL-6, but not IFN-gamma increase the expression of Cox-2, whereas they all increase the expression of HCK and FAK.
11889PTGS2ProteinHomo sapiens-eIncreases expressionindirectBCL2ProteinHomo sapiens
Forced COX-2 expression significantly attenuated TRAIL-induced apoptosis and was associated with transcriptional repression of DR-5 and up-regulation of Bcl-2.
Disease
75482CCL2ProteinHomo sapiensIncreases expressionindirectPTGS2ProteinHomo sapiens
Media as a whole, and MCP-1 alone, stimulated COX-2 expression and peripheral T cell proliferation.
163428CEBPBProteinHomo sapiens-eIncreases activitydirectPtgs2DNAMus musculus
We investigated the cis-acting elements of the COX-2 5'-flanking sequence, the transcription factors and signaling pathways responsible for transcriptional activation of the COX-2 gene in endotoxin-treated murine RAW 264.7 macrophages. / Overexpression of c-Jun, C/EBPbeta, and C/EBPdelta enhances induction of the COX-2 reporter, while overexpression of cyclic AMP-response element-binding protein or "dominant negative" C/EBPbeta represses COX-2 induction.
Structure
421527NF-kappa-BProteinRattus norvegicusIncreases expressiondirectPtgs2ProteinRattus norvegicus
Chronic ethanol intake induces brain damage, although the mechanisms involved in this effect are not well understood. / We used cerebral cortex from control and chronic ethanol-fed rats, which received ethanol-liquid diet for 5 months and cultured of astrocytes exposed to 75 mM ethanol for 7 days. Our results demonstrate that chronic ethanol treatment up-regulates iNOS, COX-2 and IL-1beta in rat cerebral cortex and in cultured astrocytes. Under both experimental conditions, up-regulation of these inflammatory mediators and IL-1RI concomitantly occurs with the stimulation of IRAK and MAP kinases, including ERK1/2, p-38 and JNK, which trigger the downstream activation of oxidant-sensitive transcription factors NF-KB and AP-1.
Regulator
421535Mapk1ProteinRattus norvegicusIncreases expressionindirectPtgs2ProteinRattus norvegicus
Chronic ethanol intake induces brain damage, although the mechanisms involved in this effect are not well understood. / We used cerebral cortex from control and chronic ethanol-fed rats, which received ethanol-liquid diet for 5 months and cultured of astrocytes exposed to 75 mM ethanol for 7 days. Our results demonstrate that chronic ethanol treatment up-regulates iNOS, COX-2 and IL-1beta in rat cerebral cortex and in cultured astrocytes. Under both experimental conditions, up-regulation of these inflammatory mediators and IL-1RI concomitantly occurs with the stimulation of IRAK and MAP kinases, including ERK1/2, p-38 and JNK, which trigger the downstream activation of oxidant-sensitive transcription factors NF-KB and AP-1.
Regulator
421539Mapk3ProteinRattus norvegicusIncreases expressionindirectPtgs2ProteinRattus norvegicus
Chronic ethanol intake induces brain damage, although the mechanisms involved in this effect are not well understood. / We used cerebral cortex from control and chronic ethanol-fed rats, which received ethanol-liquid diet for 5 months and cultured of astrocytes exposed to 75 mM ethanol for 7 days. Our results demonstrate that chronic ethanol treatment up-regulates iNOS, COX-2 and IL-1beta in rat cerebral cortex and in cultured astrocytes. Under both experimental conditions, up-regulation of these inflammatory mediators and IL-1RI concomitantly occurs with the stimulation of IRAK and MAP kinases, including ERK1/2, p-38 and JNK, which trigger the downstream activation of oxidant-sensitive transcription factors NF-KB and AP-1.
Regulator

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