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CXCL2 — NFKB1
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
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
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