Gene interactions and pathways from curated databases and text-mining

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CXCL2 — RELA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Méndez-Samperio et al., J Interferon Cytokine Res 2002 : Finally, two specific NF-kappa B inhibitors, sulfasalazine and caffeic acid phenetyl ester ( CAPE ), strongly inhibited the production of CXCL-8 by human monocytes infected with M. bovis
Chandrasekar et al., J Biol Chem 2004 (Arteriosclerosis...) : In conclusion, CXCL16 is a potent and direct activator of NF-kappaB and induces kappa B-dependent proinflammatory gene transcription
Si et al., J Immunol 2004 (Acquired Immunodeficiency Syndrome) : Interestingly, although LPS induced IL-8/CXCL8 was dependent on NF-kappaB , the baseline or 15d-PGJ ( 2 ) -mediated IL-8/CXCL8 production was NF-kappaB independent
Cinatl et al., Int J Mol Med 2005 (Colonic Neoplasms...) : High hydrocortisone concentrations ( > or =50 microg/ml ) completely prevented increased DNA binding activity of AP-1 and NF-kappaB and inhibited up-regulation of CXCL8 and CXCL10, but did not reduce chemokine expression to basal levels
Keshamouni et al., Neoplasia (New York, N.Y.) 2005 (Carcinoma, Non-Small-Cell Lung...) : Similarly, an inhibitor of NF-kappa B activation ( PDTC ) also blocked CXCL8 , CXCL5, and CXCL1 production, consistent with their NF-kappa B-dependent regulation
De Plaen et al., Immunology 2006 : LPS induced CXCL2 expression is dependent on NF-kappaB activation via the IKK pathway
Edwards et al., Mol Immunol 2007 : Focusing on CXCL8, both rhinovirus infection and dsRNA treatment required IkappaB kinase-beta for induction of CXCL8
Gupta et al., Cancer Res 2007 (Breast Neoplasms) : Suppressing Smad1 expression using small interfering RNA also mitigated MIS induced Gro-beta mRNA, suggesting that regulation of Gro-beta expression by MIS was dependent on activation of NF-kappaB as well as Smad1
D'Aversa et al., J Neurosci Res 2008 (AIDS Dementia Complex...) : Gel shift analyses demonstrated that NFkappaB and AP-1, but not C/EBPbeta, mediate microglial CXCL8 production
Yang et al., Mol Immunol 2008 (Escherichia coli Infections...) : Bovine TLR2 and TLR4 properly transduce signals from Staphylococcus aureus and E. coli, but S. aureus fails to both activate NF-kappaB in mammary epithelial cells and to quickly induce TNFalpha and interleukin-8 ( CXCL8 ) expression in the udder
Bischoff et al., J Cell Biochem 2008 : NF-kappaB inhibition resulted in a decrease in CXCL8 levels in hMSCs grown in non-OGM
Nowak et al., Mol Cell Biol 2008 : Here we find that phospho-Ser ( 276 ) RelA is required only for activation of IL-8 and Gro-beta , with IkappaBalpha being unaffected
Gregory et al., Eur J Immunol 2008 : Importantly, induction of chemokine gene expression ( MIP-2/CXCL2 , MCP-1/CCL2, MIP-1alpha/CCL3, MIP-1beta/CCL4 ) by Leishmania is NF-kappaB dependent , which implies that p35 RelA/p50 dimers are able to activate transcription, despite the absence of a recognized transcriptional transactivation domain
Martin et al., J Biol Chem 2009 : Furthermore, we identified the components of the CBM complex, Carma3, Bcl10, and Malt1, as key mediators of the CXCL8/IL8 induced NFkappaB activation and VEGF up-regulation
Ho et al., J Immunol 2009 : In contrast, NE did not induce NRF expression in A549 and Beas-2B cells, where NE only stimulates NF-kappaB activation and IL-8/CXCL8 induction
Khalaf et al., BMC immunology 2010 (Inflammation) : The present study shows that NF-kappaB regulated IL-6 but not CXCL8