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MYD88 — NFKB1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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Gene Ontology Complexes protein complex:
protein complex complex (HSF1-TRMT112-HIST1H4A-UBQLN1-CDX2-USP28-HDAC5-CAV3-CANX-LHX1-TUBA3C-TUBA3E-PI4K2A-NR0B2-RYR2-NTRK1-MPP5-N6AMT1-STAP1-ZFP42-FADD-ATP6V0D1-PRKCDBP-AQP2-FNTB-PRPSAP2-WIPI2-CRB3-CRB2-PEX11A-LDB1-RBP4-TMEM102-GATA2-ADCY2-DZIP1-SYK-TUBB4B-PTPN11-KAT5-CEP290-SYP-ASF1B-PLEKHA2-KIF24-MYO5B-RGP1-CFTR-SPTBN5-VPS72-ACTA2-PRKCI-CNST-SNX4-GNAO1-NFKBIA-UBE2D2-EPB41-RAB5A-GLUL-BSND-GSK3B-SKI-XRCC6-PPM1E-TTR-TUBA1A-SUCLG1-TRIAP1-AKT1S1-MYD88-NPPB-GDF11-INCENP-PLCB3-BECN1-PRKAB1-SOD1-TUBB1-NPHS2-NPHS1-EPS8L1-GDI1-TUBB2A-TUBB2B-SUCLG2-PEX3-TUBAL3-ERLIN1-MAGED1-GCH1-TUBB-CPS1-MEF2C-ZNF703-SLC22A6-CPLX1-EIF4EBP1-TUBE1-FLNA-CD19-STX1A-HDAC2-TOMM40L-HDAC6-SMAD6-SMAD7-TLE6-SMAD2-PARD6B-STXBP1-ACR-TRPC1-PARD6A-TRPC4-PANX1-DCTN1-SOX9-PXMP2-BCR-SET-MALT1-BHMT-RILP-TRADD-HIST1H3A-MAPK1-PVALB-NFKB1-NUFIP1-ACVR2B-TAL1-FOXP3-SSX2IP-GNB2-SLC27A5-GOPC-PAX2-CXADR-AIF1L-APBA1-MYL12A-LMO2-ID2-CCDC113-DDOST-SPP2-GATAD2B-PLN-ERCC8-BIRC8-ASF1A-CAB39-BIRC3-BIRC2-CTNNB1-CORO1A-PRELID1-HAND2-CHAF1B-SCAP-GNAT3-CDC20-SMARCA4-IQGAP1-YWHAZ-CEBPA-PRPS2-AXIN1-XRCC5-YWHAQ-UVRAG-SLC51B-RGS4-RGS6-HTT-YWHAB-APCS-CDCA8-RIPK1-MTA2-SIN3A-ANXA1-NOS1-SNTA1-TRAF6-KPNB1-VCL-VCP-PTRF-PRKCZ-SKIL-RAB3A-KRIT1-SSBP3-PRPSAP1-PPP1CC-TAB1-MYO6-ACTL7A-TUBG2-MBD2-COL6A1-COL6A2-BCL3)
Helps et al., Biochem J 2000, Lauderdale et al., Proc Natl Acad Sci U S A 2000, Didichenko et al., FEBS Lett 2000, Koh et al., Curr Biol 2002, Fan et al., Mol Cell Biol 2002, Groisman et al., Cell 2003, Offenhäuser et al., Mol Biol Cell 2004, Tagami et al., Cell 2004, Doyon et al., Mol Cell Biol 2004, Moore et al., Genomics 2004, Sun et al., Mol Cell 2004, Zang et al., J Cell Biochem 2004, Tian et al., Cancer Res 2005, An et al., Biochemistry 2005, Mahajan et al., Proc Natl Acad Sci U S A 2005, Vader et al., EMBO Rep 2006, Yeh et al., J Biol Chem 2006, Li et al., Immunol Rev 2006, Agbas et al., Biochem J 2007, Swiatecka-Urban et al., J Biol Chem 2007, McKeegan et al., Mol Cell Biol 2007, Shono et al., J Am Soc Nephrol 2007, Popov et al., Cell cycle (Georgetown, Tex.) 2007, Sato et al., J Biol Chem 2008, Fitzgerald et al., J Biol Chem 2008, Lyssand et al., J Biol Chem 2008, Figaro et al., FEBS Lett 2008, Ueda et al., Proc Natl Acad Sci U S A 2008, Shimojo et al., J Biol Chem 2008, Costantini et al., Blood 2009, Mitsuishi et al., J Biol Chem 2010, Masuda et al., J Biol Chem 2010, Koch et al., J Cell Sci 2010, Boëda et al., J Biol Chem 2011, Sircoulomb et al., EMBO Mol Med 2011, Hoxhaj et al., J Cell Sci 2012, Uckun et al., Proc Natl Acad Sci U S A 2012, Pusapati et al., J Biol Chem 2012, Ghai et al., Proc Natl Acad Sci U S A 2013, Kelly et al., PLoS Biol 2013, Chiang et al., PloS one 2013, Dauphinee et al., J Immunol 2013, Potting et al., Cell Metab 2013, Ludwig et al., PLoS Biol 2013, Lee et al., Proc Natl Acad Sci U S A 2013, Kobayashi et al., J Cell Biol 2014, Zheng et al., Am J Physiol 1994, Kumar et al., Biochem Biophys Res Commun 1998, Watabe-Uchida et al., J Cell Biol 1998, Haft et al., Mol Cell Biol 1998
Text-mined interactions from Literome
Zhang et al., FEBS Lett 2002
:
NF-kappaB activation by TLR2/1, TLR2/6 and the TLR4 monomer, but not TLR4/4, was completely
inhibited by dominant negative
MyD88 , suggesting that TLR4 homodimers and monomers could activate NF-kappaB through different mechanisms
Burns et al., J Exp Med 2003
:
In the
presence of
MyD88s , IRAK-1 is not phosphorylated and neither activates
NF-kappaB nor is ubiquitinated
Yeo et al., J Biol Chem 2003
:
Conclusively, these results demonstrate that endosomal DNA processing and
TLR9/MyD88 dependent activation of
NF-kappaB and p38 are required for transcriptional regulation of Cox-2 expression induced by CpG DNA, and suggest that interleukin-1 receptor associated kinase and/or TRAF6 may be a diverging point for NF-kappaB activation in response to CpG DNA in RAW264.7 cells
Lee et al., J Biol Chem 2003
:
Saturated fatty acid ( lauric acid ) -induced
NFkappaB activation was
inhibited by a dominant negative mutant of TLR4,
MyD88 , IRAK-1, TRAF6, or IkappaBalpha in macrophages ( RAW264.7 ) and 293T cells transfected with TLR4 and MD2 ... AKT ( DN ) blocked
MyD88 induced
NFkappaB activation, suggesting that AKT is a MyD88 dependent downstream signaling component of TLR4 ... DHA also suppressed
NFkappaB activation
induced by TLR4 ( CA ), but not
MyD88 ( CA ) or AKT ( CA ), suggesting that the molecular targets of DHA are signaling components upstream of MyD88 and AKT
Andreakos et al., Blood 2004
:
We found that
MyD88 and Mal/TIRAP are
essential for LPS induced I kappa B alpha phosphorylation,
NF-kappa B activation, and interleukin 6 (IL-6) or IL-8 production in fibroblasts and endothelial cells in a pathway that also requires IKK2 ... In contrast, in macrophages neither
MyD88 , Mal/TIRAP, nor I kappa B kinase 2 (IKK2) are
required for
NF-kappa B activation or tumor necrosis factor alpha (TNF alpha), IL-6, or IL-8 production, although Mal/TIRAP is still involved in the production of interferon beta (IFN beta)
Xiong et al., Virology 2004
:
Using a nuclear factor-kappaB (NF-kappaB) dependent reporter assay, it was shown that activation of
NF-kappaB was moderately increased in the
presence of expression of
MyD88 , and further significantly increased by co-expression of HBV
Platz et al., J Immunol 2004
:
Up-regulation of
NF-kappaB in epithelial cells in response to the CpG motif containing DNA was
inhibited by overexpression of a dominant negative form of
MyD88
Akira et al., C R Biol 2004
:
Upon stimulation, TLR recruits a cytoplasmic adaptor molecule
MyD88 , then IL-IR associated kinase ( IRAK ), and finally
induces activation of
NF-kappaB and MAP kinases
Flemming et al., Cell Immunol 2004
:
Disruption of membrane cholesterol stimulates
MyD88 dependent
NF-kappaB activation in immature B cells
Chen et al., Biochem Biophys Res Commun 2004
:
Moreover, P6 induces MUC5AC transcription via
TLR2-MyD88-IRAK1-TRAF6-TAK1 dependent p38 MAPK-AP1 and
IKKbeta-IkappaBalpha-NF-kappaB signaling pathways
Sacre et al., J Endotoxin Res 2004
:
In cell lines and murine models, parts of the signaling pathways involved have been elucidated with
MyD88 , Mal/TIRAP and IKK2 playing an important
role in the induction of
NF-kappaB ... We show that in primary human macrophages
MyD88 , Mal/TIRAP and IKK2 independent alternative pathways
activate NF-kappaB and induce the expression of inflammatory cytokines, whereas in non-myeloid synovial fibroblasts MyD88 and/or Mal/TIRAP are essential adaptors for LPS signaling
Li et al., J Mol Med (Berl) 2005
:
LPS induced, TLR4 mediated signaling employs multiple TIR-domain containing adaptors,
MyD88/TIRAP to
mediate NFkappaB activation, TRIF/TRAM for IRF3 activation
Li et al., Zhonghua Yi Xue Za Zhi 2005
(Cardiomegaly) :
MyD88 dependent
NFkappaB signaling is a novel pathway for inducing the development of cardiac hypertrophy in vivo and blocking MyD88 mediated signaling pathway attenuates the development of cardiac hypertrophy
Youn et al., J Immunol 2005
:
Further, resveratrol inhibited
NF-kappaB activation
induced by TRIF, but not by
MyD88
Carroll et al., J Immunol 2005
(Inflammation) :
In contrast, only
MyD88delta was found to
inhibit IL-1 induced
NF-kappaB reporter activity
Ness et al., J Immunol 2006
(Bacterial Infections...) :
MyD88 dependent
NF-kappaB signaling was significantly down-regulated in CCR4 ( -/- ) macrophages, whereas p38 MAPK and JNK activation were conversely increased
Koide et al., J Endotoxin Res 2007
:
LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-gamma stimulated END-D cells, although it did not affect the activation of either
MyD88 dependent
nuclear factor (NF)-kappaB or MyD88 independent IRF-3
Youn et al., Biochem Pharmacol 2008
:
Cinnamaldehyde did not inhibit the activation of
NFkappaB or IRF3
induced by
MyD88 dependent ( MyD88, IKKbeta ) or TRIF dependent ( TRIF, TBK1 ) downstream signaling components
Mizobe et al., Exp Hematol 2007
(Cell Transformation, Viral) :
In this study, we investigated whether
MyD88 , an adaptor protein of Toll-like receptor ( TLR ) signaling,
contributes to constitutive
NF-kappaB activation in HTLV-I transformed T cells ... Constitutive activation of
NF-kappaB and NF-IL-6 and cytokine gene promoters, such as IL-1alpha, interferon-gamma, and tumor necrosis factor-alpha in MT2 cells was
inhibited by
MyD88dn expression
Lin et al., Biochim Biophys Acta 2007
:
The
MyD88 activated nuclear factor-kappaB (NF-kappaB) signaling pathway and the intracellular upregulation of
NF-kappaB signaling can
induce an antiviral effect
Youn et al., Int Immunopharmacol 2008
:
Selenium inhibited
NF-kappaB activation
induced by poly [ I:C ] ( TLR3 agonist ), LPS ( TLR4 agonist ) or overexpression of
MyD88 or IKK-beta which is the key kinase of MyD88 dependent signaling pathway
Torgler et al., J Immunol 2008
(Malaria) :
Sporozoite mediated hepatocyte wounding limits Plasmodium parasite development via
MyD88 mediated
NF-kappa B activation and inducible NO synthase expression
Ahn et al., Exp Dermatol 2008
:
LPS upregulated the expression of TLR4 and
MyD88 and
induced NF-kappaB nuclear translocation B nuclear translocation in melanocytes
Lee et al., Mol Cells 2008
:
Acrolein inhibited
NF-kappaB and IRF3 activation by LPS, but it did not
inhibit NF-kappaB or IRF3 activation by
MyD88 , inhibitor kappaB kinase (IKK)beta, TRIF, or TNF-receptor associated factor family member associated NF-kappaB activator ( TANK) binding kinase 1 (TBK1 )
Hatao et al., FEMS Immunol Med Microbiol 2008
:
Expression of either a deletion mutant of
MyD88 lacking its death domain or MyD88s, neither of which induced
NF-kappaB activation , did not lead to IRAK-4 downregulation
Rallabhandi et al., J Biol Chem 2008
(Inflammation) :
In the absence of TLR4, PAR2 induced
NF-kappaB activity was
inhibited by dominant negative ( DN ) -TRIF or DN-TRAM constructs, but not by
DN-MyD88 , findings confirmed using cell-permeable, adapter-specific BB loop blocking peptides
Bhattacharyya et al., Inflamm Bowel Dis 2009
:
DSS induced increases in phospho-IkappaBalpha, nuclear
NFkappaB ( p65 ), and IL-8 secretion in human colonic epithelial cells in tissue culture are attributable to a reactive oxygen species ( ROS ) -induced pathway of inflammation, and do not
require TLR4,
MyD88 , or Bcl10, which are associated with the innate immune pathway of NFkappaB-IL-8 activation
Filipovich et al., Am J Obstet Gynecol 2009
(Escherichia coli Infections...) :
Intrauterine fetal survival, maintenance of circulating progesterone levels, and nuclear translocation of
NFkappaB were also
dependent upon
MyD88 but not TRIF
Verstak et al., J Biol Chem 2009
(Bacterial Infections...) :
MyD88 adapter-like (Mal)/TIRAP interaction with TRAF6 is
critical for TLR2- and TLR4 mediated
NF-kappaB proinflammatory responses
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
Amith et al., Cell Signal 2010
:
Here, we show that endotoxin lipopolysaccharide (LPS) induced
MyD88/TLR4 complex formation and subsequent
NFkappaB activation is dependent on the removal of alpha-2,3-sialyl residue linked to beta-galactoside of TLR4 by the Neu1 activity associated with LPS stimulated live primary macrophage cells, macrophage and dendritic cell lines but not with primary Neu1-deficient macrophage cells
Langlet et al., Eur J Immunol 2010
:
Dominant negative PKC-alpha inhibited
NF-kappaB reporter activity
mediated by overexpression of
MyD88 but not TRIF
Zheng et al., J Immunol 2010
:
In addition to promoting both
MyD88- and TLR/IL-1 receptor domain containing adaptor protein
inducing IFN-beta dependent MAPKs and
NF-kappaB activation, Gab1 enhances PI3K/Akt activation by directly binding p85 in TLR signaling and VSV infection
Li et al., Am J Nephrol 2010
(Diabetes Mellitus, Experimental...) :
The expression of TLR2 mRNA and protein level was significantly upregulated in the kidneys of diabetic rats ( p < 0.01 ), which was associated with increased renal expression of
MyD88 and MCP-1,
activation of
NF-kappaB and infiltration of macrophages
Liu et al., J Immunol 2010
:
Zebrafish
Myd88 alone strongly
induced the activation of
NF-kappaB and IFN-beta both in HEK293T and carp leukocyte cells
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
Burns et al., J Biol Chem 1998
:
Overexpression of
MyD88 induces activation of the c-Jun N-terminal kinase (JNK) and the transcription factor
NF-kappaB through its DD ...
MyD88 induced
NF-kappaB activation is inhibited by the dominant negative versions of TRAF6 and IRAK, which also inhibit IL-1 induced NF-kappaB activation ... Overexpression of MyD88-lpr or
MyD88-Toll ( expressing only the Toll domain ) acted to
inhibit IL-1 induced
NF-kappaB and JNK activation in a 293 cell line overexpressing the IL-1RI