◀ Back to NOTCH3

NFKB1 — NOTCH3

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