◀ Back to IL1A
IL1A — MYD88
Pathways - manually collected, often from reviews:
-
BioCarta nf-kb signaling pathway:
IL-1/IL-1R/MYD88/IRAK/TRAF6 complex (IL1A-IL1R1-MYD88-IRAK1-TRAF6)
→
IL-1-alpha (IL1A)
(modification, collaborate)
-
BioCarta nf-kb signaling pathway:
IL-1/IL-1R/MYD88/IRAK/TRAF6 complex (IL1A-IL1R1-MYD88-IRAK1-TRAF6)
→
IL-1R/MYD88/IRAK/TRAF6 complex (IL1R1-MYD88-IRAK1-TRAF6)
(modification, collaborate)
-
BioCarta nf-kb signaling pathway:
IL-1-alpha (IL1A)
→
IL-1R/MYD88/IRAK/TRAF6 complex (IL1R1-MYD88-IRAK1-TRAF6)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IRAKs (IRAK3/IRAK1/IRAK2)
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
TOLLIP
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IL-1-alpha (IL1A)
→
MYD88
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IL-1-alpha (IL1A)
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
MYD88
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IL-1RAcP (IL1RAP)
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IL-1RA (IL1RN)
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, inhibits)
-
BioCarta signal transduction through il1r:
IL-1R (IL1R1)
→
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
(modification, collaborate)
-
BioCarta signal transduction through il1r:
IL-1-alpha/IL-1RI/IL-1RAcP/TOLLIP/MYD88/IRAKs complex (IL1A-IL1R1-IL1RAP-MYD88-TOLLIP-IRAK3_IRAK1_IRAK2)
→
TRAF6
(modification, activates)
-
BioCarta nf-kb signaling pathway:
IL-1/IL-1R/MYD88/IRAK/TRAF6 complex (IL1A-IL1R1-MYD88-IRAK1-TRAF6)
→
TAB1/TAK1 complex (MAP3K7IP1-MAP3K7)
(modification, activates)
-
BioCarta nf-kb signaling pathway:
IL-1/IL-1R/MYD88/IRAK/TRAF6 complex (IL1A-IL1R1-MYD88-IRAK1-TRAF6)
→
IKK-alpha/MEKK1/NIK complex (CHUK-MAP3K1-MAP4K4)
(modification, activates)
-
NCI Pathway Database IL1-mediated signaling events:
MYD88 (MYD88)
→
IL1 alpha/IL1R1/IL1RAP complex (IL1A-IL1R1-IL1RAP)
(modification, collaborate)
Medzhitov et al., Mol Cell 1998*
Evidence: mutant phenotype
-
NCI Pathway Database IL1-mediated signaling events:
MYD88 (MYD88)
→
IL1 alpha/IL1R1/IL1RAP/MYD88 complex (IL1A-IL1R1-IL1RAP-MYD88)
(modification, collaborate)
Medzhitov et al., Mol Cell 1998*
Evidence: mutant phenotype
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP complex (IL1A-IL1R1-IL1RAP)
→
IL1 alpha/IL1R1/IL1RAP/MYD88 complex (IL1A-IL1R1-IL1RAP-MYD88)
(modification, collaborate)
Medzhitov et al., Mol Cell 1998*
Evidence: mutant phenotype
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4 complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4)
→
IRAK4 (IRAK4)
(modification, collaborate)
Li et al., Proc Natl Acad Sci U S A 2002
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4 complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4)
→
IL1 alpha/IL1R1/IL1RAP/MYD88 complex (IL1A-IL1R1-IL1RAP-MYD88)
(modification, collaborate)
Li et al., Proc Natl Acad Sci U S A 2002
-
NCI Pathway Database IL1-mediated signaling events:
IRAK4 (IRAK4)
→
IL1 alpha/IL1R1/IL1RAP/MYD88 complex (IL1A-IL1R1-IL1RAP-MYD88)
(modification, collaborate)
Li et al., Proc Natl Acad Sci U S A 2002
-
NCI Pathway Database IL1-mediated signaling events:
TRAF6 (TRAF6)
→
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-TOLLIP)
(modification, collaborate)
Jiang et al., Mol Cell Biol 2002, Cao et al., Nature 1996
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
TRAF6 (TRAF6)
→
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/IRAK/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-IRAK1-TOLLIP)
(modification, collaborate)
Jiang et al., Mol Cell Biol 2002, Cao et al., Nature 1996
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-TOLLIP)
→
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/IRAK/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-IRAK1-TOLLIP)
(modification, collaborate)
Jiang et al., Mol Cell Biol 2002, Cao et al., Nature 1996
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-TOLLIP)
→
IRAK/TRAF6 complex (IRAK1-TRAF6)
(modification, collaborate)
Jiang et al., Mol Cell Biol 2002, Cao et al., Nature 1996
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/IRAK/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-IRAK1-TOLLIP)
→
IRAK/TRAF6 complex (IRAK1-TRAF6)
(modification, collaborate)
Jiang et al., Mol Cell Biol 2002, Cao et al., Nature 1996
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4 complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4)
→
IRAK/TOLLIP complex (IRAK1-TOLLIP)
(modification, collaborate)
Burns et al., Nat Cell Biol 2000, Li et al., Proc Natl Acad Sci U S A 2002, Burns et al., J Exp Med 2003
-
NCI Pathway Database IL1-mediated signaling events:
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4 complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4)
→
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/IRAK/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-IRAK1-TOLLIP)
(modification, collaborate)
Burns et al., Nat Cell Biol 2000, Li et al., Proc Natl Acad Sci U S A 2002, Burns et al., J Exp Med 2003
-
NCI Pathway Database IL1-mediated signaling events:
IRAK/TOLLIP complex (IRAK1-TOLLIP)
→
IL1 alpha/IL1R1/IL1RAP/MYD88/IRAK4/IRAK/TOLLIP complex (IL1A-IL1R1-IL1RAP-MYD88-IRAK4-IRAK1-TOLLIP)
(modification, collaborate)
Burns et al., Nat Cell Biol 2000, Li et al., Proc Natl Acad Sci U S A 2002, Burns et al., J Exp Med 2003
-
Reactome Reaction:
IL1A
→
MYD88
(reaction)
Li et al., Proc Natl Acad Sci U S A 2002, Kollewe et al., J Biol Chem 2004, Brikos et al., Mol Cell Proteomics 2007*, Wesche et al., Immunity 1997
-
Reactome Reaction:
IL1A
→
MYD88
(indirect_complex)
Cheng et al., Biochem Biophys Res Commun 2007, Brikos et al., Mol Cell Proteomics 2007*, Wesche et al., Immunity 1997
Text-mined interactions from Literome
Medvedev et al., J Immunol 2005
(Bacterial Infections...) :
Thus, decreased IL-1 induced association of IRAK-1 and MyD88 with the
IL-1RI may
result from sequestration of cytoplasmic
MyD88 by IRAK-4 mutant proteins
Togbe et al., Lab Invest 2006
:
However, the relative roles of the TLR4 adaptor proteins TIRAP and TRIF and of the
MyD88 dependent
IL-1 and IL-18 receptor pathways in this response are unclear
Rad et al., Gastroenterology 2007
(Gastritis...) :
The adaptor protein
Myd88 mediates Toll-like receptor ( TLR ),
interleukin (IL)-1 , and IL-18 signaling
von Bernuth et al., Science 2008
(Bacterial Infections...) :
The
MyD88 dependent TLRs and
IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections
Zhou et al., J Virol 2009
(Arenaviridae Infections) :
This effect was not the result of
MyD88 regulation of
IL-1 or IL-18 responses since IL-1R1 KO and IL-18R KO mice were not protected from weight loss
Kissner et al., Innate Immun 2011
(Disease Models, Animal...) :
Our results indicated that elevated tumor necrosis factor-a, interferon-?,
interleukin (IL)-1a/ß and IL-6 production from mouse spleen cells treated with SEB alone or in combination with lipopolysaccharide (LPS) was
regulated by
MyD88
Huang et al., J Immunol 2010
(Inflammation...) :
IL-1ß and IL-18 secretion was dependent on inflammasome components pyrin-caspase recruitment domain/apoptotic speck containing protein with a caspase recruitment domain and caspase-1, and the TLR/IL-1R signaling molecule
MyD88 was
required for inflammatory cytokine synthesis
Ather et al., J Immunol 2011
(Disease Models, Animal...) :
Furthermore, SAA drives production of IL-1a,
IL-1ß , IL-6, IL-23, and PGE ( 2 ), causes dendritic cell ( DC ) maturation, and
requires TLR2,
MyD88 , and the NLRP3 inflammasome for secretion of IL-1ß by DCs and macrophages
Shimada et al., PloS one 2011
(Chlamydia Infections...) :
In vitro investigation reveals that CP-induced
IL-1ß secretion by macrophages
requires TLR2/MyD88 and NLRP3/ASC/Caspase-1 signaling
Guerrero et al., Eur J Pharmacol 2012
:
Moreover, the joint production of TNF-a,
IL-1ß and CXCL1/KC by zymosan was
dependent on
TLR2/MyD88 signaling
Madera et al., PloS one 2011
:
R-848 activation of Toll-like receptor
7/MyD88 dependent signaling in cDCs
led to a rapid upregulation of pro-IL-1a and
pro-IL-1ß production compared to poly I:C activation of MyD88 independent signaling pathways
Segovia et al., PloS one 2012
(Respiratory Syncytial Virus Infections) :
TLR2/MyD88/NF-?B signaling is
required for
pro-IL-1ß and NLRP3 gene expression during RSV infection
Ouziel et al., Am J Pathol 2012
(Acute Disease...) :
Activation of
interleukin 1ß (IL-1ß) and immunomodulation via
MyD88 , the first signaling molecule in the ST2 pathway, seem to be involved
Kavathas et al., Mucosal Immunol 2013
:
In addition, we demonstrate that Ct-induced
IL-1ß production and secretion by the trophoblast is
independent of TLR2, TLR4,
MyD88 , and the Nalp3/ASC inflammasome
Ogura et al., Pathogens and disease 2013
:
At higher concentrations, Escherichia coli-type hexa acylated lipid A 506, Salmonella-type hepta acylated lipid A 516, the lipid A precursor lipid IVa and monophosphoryl lipid A induced similar levels of production of the
MyD88 dependent cytokine
IL-1ß although their potencies varied, whereas the maximum production of the MyD88 independent cytokine RANTES induced by lipid IVa was less than 50 % that of other lipid A compounds
Wesche et al., Immunity 1997
:
Thus,
MyD88 plays the same role in
IL-1 signaling as TRADD and Tube do in TNF and Toll pathways, respectively : it couples a serine/threonine protein kinase to the receptor complex