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NOTCH2 — RELA
Text-mined interactions from Literome
Wang et al., J Immunol 2001
:
We found that
Notch ( IC ) localizes to the nucleus and that a region in the N-terminal portion of Notch ( IC ), not the six ankyrin repeats, is
responsible for the inhibitory effects of Notch on NF-kappaB directed gene expression and
NF-kappaB DNA binding activity
Palaga et al., J Immunol 2003
:
Inhibition of
Notch activation dramatically decreases T cell proliferation in both CD4 and CD8 cells and
blocks both
NF-kappaB activity and IFN-gamma production in peripheral T cells
Shin et al., EMBO J 2006
:
Here, we examined the temporal relationship between
Notch signaling and
NF-kappaB induction during T-cell activation
Wang et al., Mol Cancer Ther 2006
(Pancreatic Neoplasms) :
Because Notch-1 is known to cross-talk with another major cell growth and apoptotic regulatory pathway ( i.e., NF-kappaB ), we found that NF-kappaB is a downstream target of Notch because down-regulation of
Notch reduced
NF-kappaB activity
Palaga et al., Eur J Immunol 2008
:
Taken together, stimulation of macrophages through the TLR signaling cascade triggered
activation of
Notch signaling, which in turn regulated gene expression patterns involved in pro-inflammatory responses, through activation of
NF-kappaB
Mandinova et al., EMBO J 2008
:
Conversely, Notch activation protects keratinocytes against apoptosis through a mechanism that is not linked to
Notch induced cell cycle withdrawal or
NF-kappaB activation
Monsalve et al., Eur J Immunol 2009
:
We report here that
Notch signaling
increases both basal and LPS induced
NF-kappaB activation, favoring the expression of genes implicated in the inflammatory response, such as the cytokines TNF-alpha and IL-6, or enzymes, such as iNOS