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RELA — TACR1
Text-mined interactions from Literome
Zhao et al., Biochem J 2002
:
However, the signalling mechanisms by which
SP-NK-1R interaction
induces NF-kappaB activation and IL-8 expression are still not clear
Weinstock et al., J Immunol 2003
:
Inhibition of T cell
NF-kappa B activation or NF-kappa B nuclear translocation also
blocked NK-1R transcription
Koon et al., J Pharmacol Exp Ther 2005
:
However, the signal transduction pathways by which
SP-NK-1R interaction
induces NF-kappaB activation and interleukin-8 (IL-8) production are not clear
Reed et al., Dig Dis Sci 2005
(Colitis...) :
Colon tissue was collected for assessment of histological changes,
NF-kappa B activation , myeloperoxidase (MPO) activity, and expression of
NK-1R , SP, TNFalpha, IL-1beta, VCAM-1, ICAM-1, E-selectin, CINC-1, MIP-1alpha, and iNOS
Williams et al., Am J Physiol Lung Cell Mol Physiol 2007
:
Expression of inhibitory peptides and constitutively active G protein mutants revealed that G ( q ) signaling was both necessary for
Tacr1 induced
NF-kappaB activation and sufficient for NF-kappaB activation in the absence of any other treatment ... Treatment with pharmacological inhibitors to investigate events downstream of G ( q ) revealed that
Tacr1 induced
NF-kappaB activation proceeded through an intracellular signaling pathway that was dependent on phospholipase C, calcium, Ras, Raf-1, MEK, Erk, and proteasome function
Saban et al., BMC urology 2007
(Cystitis) :
Electrophoretic mobility shift assays confirmed that, in the mouse urinary bladder, activation of
NK1R by substance P ( SP )
induces both NKx-2.5 and
NF-kappaB translocations
Ramnath et al., Am J Physiol Cell Physiol 2008
:
However, the signaling mechanisms by which the
SP-NK1R interaction
induces NF-kappaB activation and chemokine production remain unclear
Xu et al., Exp Lung Res 2010
:
To evaluate the direct effects of CS and SP on the NK1R expression and the involvement of nuclear factor (NF)-kappaB, macrophages were exposed to CS condensate ( CSC ) and/or SP without or with blocking
NK1R or
inhibiting NF-kappaB activation in vitro