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IL1R1 — RELA
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Schwenzer et al., J Biol Chem 1999
:
Because it has been shown that members of the TRAF family are involved in
activation of
NF-kappaB and the c-Jun N-terminal kinase (JNK) by the
interleukin-1 receptor and members of the TNF receptor superfamily, a role of TRAF1 in receptor cross-talk and/or feedback regulation of activated receptor signaling complexes can be suggested
Janssens et al., FEBS Lett 2003
:
MyD88 is an adapter protein that is involved in Toll-like receptor ( TLR ) - and
interleukin-1 receptor (IL-1R) induced activation of
nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) ... MyD88 ( S ) is not able to activate NF-kappaB, and in contrast functions as a dominant negative inhibitor of
TLR/IL-1R induced
NF-kappaB activation
Kitagawa et al., Am J Physiol Gastrointest Liver Physiol 2004
:
Our results indicate that EGF and IL-1beta stimulate two essential signals for iNOS induction in IEC-6 cells : the upregulation of
IL-1R1 through PI3-kinase/Akt and the
activation of
NF-kappaB through IkappaB kinase, respectively
Wang et al., Nat Immunol 2006
:
Tumor necrosis factor receptor associated factor 6 ( TRAF6 ) is critical for mediating Toll-like receptor ( TLR )
-interleukin 1 receptor (IL-1R) signaling and subsequent
activation of
NF-kappaB and AP-1, transcriptional activators of innate immunity
Fraczek et al., J Biol Chem 2008
:
Two parallel interleukin-1 (IL-1) mediated signaling pathways have been uncovered for
IL-1R-TLR mediated
NFkappaB activation : TAK1 dependent and MEKK3 dependent pathways, respectively ... Deletion analysis of IRAK4 indicates the essential structural role of the IRAK4 death domain in receptor proximal signaling for mediating
IL-1R-TLR induced
NFkappaB activation
Loiarro et al., J Biol Chem 2009
:
Moreover, overexpression of a green fluorescent protein ( GFP ) -tagged mini-MyD88 protein ( GFP-MyD88- ( 27-72 ) ), comprising the Glu ( 52 ) and Tyr ( 58 ) residues, interfered with recruitment of both IRAK1 and IRAK4 by MyD88 and suppressed
NF-kappaB activation by the
interleukin-1 receptor but not by the MyD88 independent TLR3
Lee et al., Biochim Biophys Acta 2009
:
DSCR1-1S also stimulated
IL-1R mediated signaling pathways, TAK1 activation,
NF-kappaB transactivation, and IL-8 production, all downstream consequences of IL-1R activation
Kissner et al., PloS one 2011
(Inflammation) :
Here we report that human monocytes treated with SEA, SEB, or anti-MHC class II monoclonal antibodies up regulated MyD88 expression, induced
activation of
NF-kB , and increased expression of
IL-1R1 accessory protein, TNF-a and IL-1ß
Muzio et al., Science 1997
:
Two additional proximal mediators were identified that are required for
IL-1R induced
NF-kappaB activation : IRAK-2, a Pelle family member, and MyD88, a death domain containing adapter molecule ... Dominant negative forms of either attenuate
IL-1R mediated
NF-kappaB activation