Gene interactions and pathways from curated databases and text-mining

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CXCL1 — RELA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Devalaraja et al., Cancer Res 1999 (Melanoma) : We also show here that the resultant elevated nuclear NF-kappaB ( p50/p65 ) in these cells is responsible for the increased basal transcription of MGSA/GRO-alpha ... Cotransfection of a 350-bp MGSA/GRO-alpha promoter-luciferase reporter construct with either the dominant negative IKK-alpha or the repressors of NF-kappaB, the IkappaB-alpha wild type or mutants lacking the inducible phosphorylation sites, demonstrates that the increased basal MGSA/GRO-alpha transcription in the Hs294T cells is due to the enhanced nuclear activation of NF-kappaB
Wang et al., J Biol Chem 2001 (Cell Transformation, Neoplastic) : We show here that either exogenous addition or continuous expression of MGSA/GROalpha in immortalized melanocytes enhances NF-kappaB activation, as well as mitogen activated protein ( MAP ) kinase kinase kinase ( MEKK) 1, MAP kinase kinase (MEK) 3/6, and p38 MAP kinase activation ... Expression of dominant negative M-Ras ( S27N ), dominant negative MEKK1 ( K432M ), or specific chemical inhibitors for p38 MAP kinase ( SB202190 and SB203580 ) block MGSA/GROalpha induced NF-kappaB transactivation, demonstrating that Ras, MEKK1, and p38 are involved in the signal pathways of MGSA/GROalpha activation of NF-kappaB
Loukinova et al., Int J Cancer 2001 (Carcinoma, Squamous Cell...) : The enhanced expression of Gro-1 gene by SCC is regulated by activation of nuclear factor-kappaB (NF-kappaB) , leading to accelerated tumor growth, angiogenesis and metastasis in vivo
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
Edwards et al., Mol Immunol 2007 : Focusing on CXCL8, both rhinovirus infection and dsRNA treatment required IkappaB kinase-beta for induction of CXCL8
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
Bachmeier et al., Carcinogenesis 2008 (Breast Neoplasms) : Using small interfering RNA techniques, we elucidated the underlying molecular mechanism revealing that reduction of CXCL1 and -2 messenger RNA levels is NFkappaB dependent and requires intact IkappaBalpha expression
Bischoff et al., J Cell Biochem 2008 : NF-kappaB inhibition resulted in a decrease in CXCL8 levels in hMSCs grown in non-OGM
Guillot et al., Infect Immun 2008 (Cryptococcosis...) : Intracellular signaling analysis demonstrated that TNF-alpha and KC/CXCL1 production was regulated by NF-kappaB and phosphatidylinositol 3 kinase in both strains ; however, SJL/J macrophages exhibited heightened and prolonged activation in response to C. neoformans infection compared to that of C57BL/6J
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
Le Dréau et al., Glia 2010 : Using a panel of kinase inhibitors, we demonstrated that NOV action on CCL2 and CXCL1 production involved a Rho/ROCK/JNK/NF-kappaB and a Rho/qROCK/p38/NF-kappaB pathway, respectively
Wood et al., J Biol Chem 1995 (Melanoma) : Constitutive and cytokine induced expression of the melanoma growth stimulatory activity/GRO alpha gene requires both NF-kappa B and novel constitutive factors
Luan et al., J Leukoc Biol 1997 (Disease Progression...) : We propose that this endogenous nuclear NF-kappaB , working in concert with the 115-kDa IUR binding factor, promotes constitutive expression of MGSA/GRO genes