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IKBKB — IL8
Text-mined interactions from Literome
Li et al., J Exp Med 1999
:
Accordingly, IKKbeta-deficient cells are defective in activation of
IKK and NF-kappaB in
response to either tumor necrosis factor alpha or
interleukin 1
Wang et al., Infect Immun 2001
:
These data indicate that micrococci and PGN induce TLR2 dependent activation of the gene for
IL-8 and that this activation
requires MyD88, IRAK, NIK,
IKK , and NF-kappaB and may also utilize TRAF6 and, to a lesser extent, TRAF2
Casola et al., Virology 2002
:
Rotavirus infection of HT-29 induced IkappaB kinase (IKK) activation and overexpression of a dominant negative mutant of IKK-beta greatly reduced rotavirus induced IL-8 promoter activation and NF-kappaB-driven transcription, indicating that
IKK is
involved in rotavirus induced
IL-8 gene expression and NF-kappaB activation
Andreakos et al., Blood 2004
:
In contrast, in macrophages neither MyD88, Mal/TIRAP, nor
I kappa B kinase 2 (IKK2) are
required for NF-kappa B activation or tumor necrosis factor alpha (TNF alpha), IL-6, or
IL-8 production, although Mal/TIRAP is still involved in the production of interferon beta (IFN beta)
Podolin et al., J Pharmacol Exp Ther 2005
(Arthritis, Experimental...) :
In the present study, we demonstrate that a novel, potent ( IC ( 50 ) = 17.9 nM ), and selective inhibitor of human
IKK-2 , 2- [ ( aminocarbonyl ) amino ] -5- ( 4-fluorophenyl ) -3-thiophenecarboxamide ( TPCA-1 ),
inhibits lipopolysaccharide induced human monocyte production of TNF-alpha, IL-6, and
IL-8 with an IC ( 50 ) = 170 to 320 nM
Catley et al., Br J Pharmacol 2005
(Asthma) :
Similarly,
IKK beta ( KA ) and I kappa B alpha delta N overexpression also
inhibited IL-1beta- and TNF alpha dependent increases in ICAM-1,
IL-8 and GM-CSF in addition to IL-1beta mediated increases in cyclooxygenase-2 expression, whereas IKK alpha ( KM ) overexpression had little effect on these outputs
Catley et al., Mol Pharmacol 2006
(Pulmonary Disease, Chronic Obstructive) :
As observed above, ICAM-1, IL-6,
IL-8 , GM-CSF, RANTES, MCP-1, GROalpha, NAP-2, and ENA-78 expression was
reduced by the
IKK inhibitors
Lamothe et al., J Biol Chem 2007
:
Reconstituting TRAF6-deficent cells with various TRAF6 mutants, we clearly demonstrate the requirement for the TRAF6 RING domain and site-specific auto-ubiquitination of TRAF6 to activate
IKK in
response to
interleukin-1
Grund et al., Mol Pharmacol 2008
(Endometriosis...) :
Interestingly, MEK, p38, and
IKK inhibitors
block TNF-alpha induced
IL-8 , IL-6, and GM-CSF secretion and 12z invasion, whereas the PI3K inhibitors do not
Shah et al., Journal of neuroinflammation 2010
:
We have also shown that the NF-?B pathway is involved in gp120 mediated IL-8 overexpression as
IKK-2 and IKKß inhibitors
inhibited IL-8 expression by 63.5 % and 57.5 %, respectively at the mRNA level, and by 67.3 % and 58.6 % at the protein level
Sachse et al., Rhinology 2011
(Nasal Polyps) :
IL-8 and GRO-a responses were
repressed by
IKK-2 inhibitor TPCA-1 in vitro
Du et al., J Interferon Cytokine Res 2012
(Glioma) :
IKK inhibitors
inhibit glioma cell proliferation, as well as TNF induced RelA ( p65 ) nuclear translocation and NF?B dependent
IL8 gene expression
O'Connell et al., J Biol Chem 1998
:
Recently, we have reported that the tumor necrosis factor and
interleukin 1 signaling pathways
activate two kinases,
IKK1 and IKK2 ... Recently, we have reported that the tumor necrosis factor and
interleukin 1 signaling pathways
activate two kinases, IKK1 and
IKK2