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IKBKE — RELA
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
RELA
→
IKBKE
(directlyIncreases, RELA Activity)
Evidence: 10521409;15128824;15849198;15489227;15485852;12767944
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
IKBKE
—
RELA
(direct interaction, enzymatic study)
Buss et al., J Biol Chem 2004*
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MIPS CORUM TNF-alpha/NF-kappa B signaling complex (CHUK, BTRC, NFKB2, PPP6C, REL, CUL1, IKBKE, SAPS2, SAPS1, ANKRD28, RELA, SKP1):
TNF-alpha/NF-kappa B signaling complex (CHUK, BTRC, NFKB2, PPP6C, REL, CUL1, IKBKE, SAPS2, SAPS1, ANKRD28, RELA, SKP1) complex (ANKRD28-BTRC-CHUK-CUL1-IKBKE-NFKB2-PPP6C-REL-RELA-PPP6R1-PPP6R2-SKP1)
Bouwmeester et al., Nat Cell Biol 2004
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IRef Corum Interaction:
Complex of 13 proteins
(association, tandem affinity purification)
Bouwmeester et al., Nat Cell Biol 2004
-
IRef Hprd Interaction:
Complex of 170 proteins
(in vivo)
Bouwmeester et al., Nat Cell Biol 2004
Text-mined interactions from Literome
Shimada et al., Int Immunol 1999
(Inflammation) :
Overexpression of wild-type
IKK-i phosphorylated serine residues Ser32 and Ser36 of IkappaB-alpha ( preferentially Ser36 ), and significantly
stimulated NF-kappaB activation
Nomura et al., Genes Cells 2000
:
IKK-i significantly
induced NF-kappaB activation upon over-expression, as did IKK-alpha and IKK-beta ...
NF-kappaB activation by
IKK-i is significantly blocked by coexpression of the N-terminal domain of I-TRAF, dominant negative TRAF2, and dominant negative NIK and IKK-beta ...
NF-kappaB activation by
IKK-i may be mediated through phosphorylation of I-TRAF by IKK-i and subsequent liberation of TRAF2 ... These results indicate that
NF-kappaB activation by
IKK-i is mediated through phosphorylation of I-TRAF/TANK by IKK-i and subsequent liberation of TRAF2
Wang et al., FEBS Lett 2004
:
A20 also inhibited TRIF-, but not its downstream signaling components TBK1-, IKKbeta-, and
IKKepsilon mediated activation of ISRE and
NF-kappaB and IFN-beta promoter
Sankar et al., Cell Signal 2006
:
Our data suggest that expression of
IKK-i can
activate both
NFkappaB and IRF3, leading to the production of several cytokines including interferon beta
Eddy et al., Cancer Res 2005
(Breast Neoplasms) :
Expression of a kinase-inactive
IKK-i/IKKepsilon mutant in breast cancer cells
reduced NF-kappaB activity as judged by transfection assays of reporters driven either by NF-kappaB elements or the promoters of two NF-kappaB target genes, cyclin D1 and relB
Adli et al., J Biol Chem 2006
(Inflammation) :
Here, we demonstrate that
IKK-i/IKKepsilon is expressed in a number of cancer cells and is
involved in regulating
NF-kappaB activity through its ability to control basal/constitutive, but not cytokine induced, p65/RelA phosphorylation at Ser-536, a modification proposed to contribute to the transactivation function of NF-kappaB