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NFKB1 — TSC22D3
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Ayroldi et al., Mol Cell Biol 2002
(MAP Kinase Signaling System) :
In fact,
GILZ overexpression
inhibits TCR activated
NF-kappaB nuclear translocation, interleukin-2 production, FasL upregulation, and the consequent activation induced apoptosis
Di Marco et al., Nucleic Acids Res 2007
:
We have previously shown that
GILZ binds to and
inhibits NF-kappaB activity
Bai et al., Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2007
(Inflammation) :
Overexpression of
GILZ inhibits
NF-KappaB and AP-1 activities, suggesting that GILZ possesses anti-inflammatory function
Eddleston et al., J Allergy Clin Immunol 2007
:
Overexpression of
GILZ in BEAS-2B cells significantly
inhibited the ability of IL-1beta, LPS, and polyinosinic : polycytidylic acid to activate
NF-kappaB , whereas knockdown of GILZ inhibited the ability of dexamethasone to suppress IL-1beta induced chemokine expression
Yang et al., J Immunol 2009
:
GC-induced
GILZ expression and GC
inhibition of
NF-kappaB activation were restored by expression of ANXA1 in ANXA1 ( -/- ) cells, and GILZ overexpression in ANXA1 ( -/- ) macrophages reduced ERK MAPK phosphorylation and restored sensitivity of cytokine expression and NF-kappaB activation to GC
Ayroldi et al., FASEB J 2009
:
The identification of
GILZ interaction with and
inhibition of
NF-kappaB provided a first molecular mechanistic basis for explaining GILZ effects on T cells