PMID: 16920490
IFN-gamma binds to the IFN-gamma receptor.
indirect
PMID: 16920490, 11964313, 12811837,7999637, 11672593, 12831455
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
indirect
PMID: 16920490, 12831455, 11672593, 7999637, 12811837, 11964313
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
indirect
PMID: 16920490, 11964313, 12811837, 7999637, 1167259
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
indirect
PMID: 16920490, 12831455, 11672593, 7999637, 12811837, 11964313
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
indirect
PMID: 16920490, 11964313, 12811837, 7999637, 11672593, 12831455
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
PMID: 16920490, 11964313, 12811837, 7999637, 11672593, 12831455
IFNγ stimulation induced Tlr2, Tlr4, and Tlr6 mRNAs, upregulated expression of TLR2 and TLR4 protein at the cell surface, and increased resulting LPS-binding ability of macrophages
PMID: 16920490, 1698311
In the case of LPS, efficient ligand recognition requires the signalling receptor TLR4, as well as the CD14 co-receptor
PMID: 16920490, 1698311, 10359581
In the case of LPS, efficient ligand recognition requires the signalling receptor TLR4, as well as the CD14 co-receptor (Wright et al., 1990) and MD-2 accessory molecule
PMID: 16920490, 1698311, 10359581
n the case of LPS, efficient ligand recognition requires the signalling receptor TLR4, as well as the CD14 co-receptor (Wright et al., 1990) and MD-2 accessory molecule
PMID: 16920490, 14993454
Full signal transduction requires a number of signalling adaptors, including MyD88 and the adaptors of the MyD88-independent pathway, TRAM (also called TIRP, TICAM2) and TRIF (also known as TICAM1) (reviewed in Vogel et al., 2003)
PMID: 16920490, 14993454
Full signal transduction requires a number of signalling adaptors, including MyD88 and the adaptors of the MyD88-independent pathway, TRAM (also called TIRP, TICAM2) and TRIF (also known as TICAM1) (reviewed in Vogel et al., 2003)
PMID: 16920490, 14993454
Full signal transduction requires a number of signalling adaptors, including MyD88 and the adaptors of the MyD88-independent pathway, TRAM (also called TIRP, TICAM2) and TRIF (also known as TICAM1) (reviewed in Vogel et al., 2003)
PMID: 16920490, 11130078
CpG DNA signalling is mediated by the TLR9 signalling receptor
PMID: 16920490, 11130078
CpG DNA signalling is mediated by the TLR9 signalling receptor (Hemmi et al., 2000), and unlike TLR4, the MyD88 signalling adaptor mediates all known downstream responses (Schnare et al., 2000).
indirect
PMID: 16920490, 15928677
LPS induces expression of negative regulators of key adaptor/signalling molecules (e.g. IRAK-M and SOCS1 that target IRAKs, ST2L that sequesters MyD88 and MAL) (Liew et al., 2005).
indirect
PMID: 16920490, 15928677, 11870615, 12811837, 10453004
LPS induces expression of negative regulators of key adaptor/signalling molecules (e.g. IRAK-M and SOCS1 that target IRAKs, ST2L that sequesters MyD88 and MAL) (Liew et al., 2005).
Both LPS and IFNγ induced expression of these SOCS proteins (SOCS1 and SOCS3), and LPS pre-treatment inhibited some functions of IFNγ signalling via the activities of these proteins (Crespo et al., 2002; Dalpke et al., 2003; Stoiber et al., 1999
indirect
indirect
PMID: 16920490
Induction of Tlr9 mRNA by IFNγ in BMM was largely dependent on the presence of CSF-1 that suppressed Tlr9 expression (manuscript in preparation).
PMID: 16920490
Induction of Tlr9 mRNA by IFNγ in BMM was largely dependent on the presence of CSF-1 that suppressed Tlr9 expression (manuscript in preparation).
PMID: 16920490, 10725699
LPS downregulates surface expression of the signalling receptor TLR4, and its accessory molecule, MD-2 (Nomura et al., 2000).
PMID: 16920490, 10725699
LPS downregulates surface expression of the signalling receptor TLR4, and its accessory molecule, MD-2 (Nomura et al., 2000).
indirect
PMID: 16920490, 11964313, 15324355, 12761135,12831455
Numerous reports document the IFNγ-dependent induction of the CD14 co-receptor and MD-2 accessory molecule, which aid in LPS signalling
indirect
PMID: 16920490, 12831455, 12761135, 15324355 ,11964313
Numerous reports document the IFNγ-dependent induction of the CD14 co-receptor and MD-2 accessory molecule, which aid in LPS signalling
indirect
PMID: 16920490, 11964313, 15324355, 12761135, 12831455
12032143
Additionally, IFNγ upregulated the expression of MyD88 (Bosisio et al., 2002; Mochizuki et al., 2004; Tamai et al., 2003) and IRAK1 (Adib-Conquy and Cavaillon, 2002), which participate in TLR signalling pathways.
indirect
PMID: 16920490,12032143
Additionally, IFNγ upregulated the expression of MyD88 and IRAK1
indirect
PMID: 16920490, 12811837, 10453004, 11870615
Both LPS and IFNγ induced expression of these SOCS proteins (SOCS1 and SOCS3), and LPS pre-treatment inhibited some functions of IFNγ signalling via the activities of these proteins (Crespo et al., 2002; Dalpke et al., 2003; Stoiber et al., 1999).
indirect
PMID: 16920490, 11870615, 10453004, 12811837
Both LPS and IFNγ induced expression of these SOCS proteins (SOCS1 and SOCS3), and LPS pre-treatment inhibited some functions of IFNγ signalling via the activities of these proteins (Crespo et al., 2002; Dalpke et al., 2003; Stoiber et al., 1999).
indirect
PMID: 16920490, 10453004, 12811837, 11870615
Both LPS and IFNγ induced expression of these SOCS proteins (SOCS1 and SOCS3), and LPS pre-treatment inhibited some functions of IFNγ signalling via the activities of these proteins (Crespo et al., 2002; Dalpke et al., 2003; Stoiber et al., 1999
indirect
PMID: 16920490, 15928677
LPS induces expression of negative regulators of key adaptor/signalling molecules (e.g. IRAK-M and SOCS1 that target IRAKs, ST2L that sequesters MyD88 and MAL) (Liew et al., 2005).
PMID: 16920490, 9864217
IFNγ pre-treatment of RAW264.7 cells promoted LPS-induced NF-κB activation and DNA binding kinetics, as well as causing more rapid degradation of the NF-κB inhibitor, IκBα (Held et al., 1999)
indirect
PMID: 16920490, 9864217
IFNγ pre-treatment of RAW264.7 cells promoted LPS-induced NF-κB activation and DNA binding kinetics, as well as causing more rapid degradation of the NF-κB inhibitor, IκBα (Held et al., 1999)
indirect
PMID: 16920490
IFNγ also influenced the activity of another key LPS-induced transcription factor, AP-1, in human monocytes.
indirect
PMID: 16920490, 11972023, 10975834, 9649436
In the case of TLR4, LPS treatment following IFNγ exposure increased the percentage of STAT1 molecules phosphorylated on both Y701 and S727, and subsequent STAT1 DNA-binding activity relative to IFNγ treatment alone
Indirect
PMID: 16920490, 12667213, 9568729
IFNγ signalling induced Inos mRNA via STAT1, but induction was maximal only when the Inos promoter NF-κB sites were occupied following TLR ligation
Indirect
PMID: 16920490, 2498530
IFN-gamma stimulation induces Ifn-beta mRNA.
PMID: 16920490, 12811837, 12686553
Signalling initiated by a number of TLR agonists (e.g. LPS, CpG DNA, lipotechoic acid) induced STAT1 S727 phosphorylation, via activation of p38 MAPK pathways (
indirect
PMID: 16920490, 12811837, 12686553
Signalling initiated by a number of TLR agonists (e.g. LPS, CpG DNA, lipotechoic acid) induced STAT1 S727 phosphorylation, via activation of p38 MAPK pathways
indirect
PMID: 16920490, 12811837, 12686553
Signalling initiated by a number of TLR agonists (e.g. LPS, CpG DNA, lipotechoic acid) induced STAT1 S727 phosphorylation, via activation of p38 MAPK pathways
indirect
PMID: 16920490, 12811837, 12686553
Signalling initiated by a number of TLR agonists (e.g. LPS, CpG DNA, lipotechoic acid) induced STAT1 S727 phosphorylation, via activation of p38 MAPK pathways
PMID: 16920490, 12811837, 12686553
Signalling initiated by a number of TLR agonists (e.g. LPS, CpG DNA, lipotechoic acid) induced STAT1 S727 phosphorylation, via activation of p38 MAPK pathways
PMID: 16920490, 10975834, 9649436
In the case of TLR4, LPS treatment following IFNγ exposure increased the percentage of STAT1 molecules phosphorylated on both Y701 and S727, and subsequent STAT1 DNA-binding activity relative to IFNγ treatment alone
PMID: 16920490, 10975834, 9649436
In the case of TLR4, LPS treatment following IFNγ exposure increased the percentage of STAT1 molecules phosphorylated on both Y701 and S727, and subsequent STAT1 DNA-binding activity relative to IFNγ treatment alone
indirect
PMID: 16920490, 16816106
Recent studies from our laboratory showed that Hdac1 mRNA was induced by LPS in BMM and that HDACs acted as negative feedback regulators of a sub-set of LPS-inducible genes, including Cox2
PMID: 16920490, 16816106
Recent studies from our laboratory showed that Hdac1 mRNA was induced by LPS in BMM and that HDACs acted as negative feedback regulators of a sub-set of LPS-inducible genes, including Cox2
PMID: 16920490, 14645718, 16481475
Further, STAT1 and HDAC1 physically interact (Nusinzon and Horvath, 2003) and STAT1 is an acetylated protein
indirect
PMID: 16920490, 16816106
Recent studies from our laboratory showed that Hdac1 mRNA was induced by LPS in BMM and that HDACs acted as negative feedback regulators of a sub-set of LPS-inducible genes, including Cox2
indirect
PMID: 14920490, 16164016
Both IFNγ and LPS induce Icsbp mRNA in macrophages, but induction is dependent on the presence of CSF-1
Coupled with the studies from our laboratory described above, demonstrating that ICSBP expression was modulated by both IFNγ (positively) and CSF-1 (negatively), this implies that ICSBP functions to integrate CSF-1 and IFNγ signalling directly into the TLR signalling pathway, by directly modulating TRAF6 function.
indirect
PMID: 16920490, 16164016
Both IFNγ and LPS induce Icsbp mRNA in macrophages, but induction is dependent on the presence of CSF-1
PMID:16920490, 8456286, 16484229
S148-phosphorylated PU.1 is able to interact with ICSBP upon composite PU.1/IRF sites to potentiate PU.1-dependent transactivation
the Ets family member PU.l is phosphorylated by LPS and interacts with IFNγ-induced ICSBP
ICSBP may participate more directly in the TLR signalling pathway, via interaction with TRAF6
PMID: 14920490, 16484229
In addition to its function as a transcription factor, a recent article suggested that ICSBP may participate more directly in the TLR signalling pathway, via interaction with TRAF6
indirect
PMID: 16920490, 7609733
PU.1 is phosphorylated at S148 in response to LPS, and phosphorylation is necessary for the full spectrum of macrophage responses to LPS (e.g. induction of IL-1β (Buras et al., 1995)
PMID: 16920490, 8456286,1729611
S148-phosphorylated PU.1 is able to interact with ICSBP upon composite PU.1/IRF sites to potentiate PU.1-dependent transactivation
the Ets family member PU.l is phosphorylated by LPS and interacts with IFNγ-induced ICSBP
PMID: 16920490, 9864217
IFNγ pre-treatment of RAW264.7 cells promoted LPS-induced NF-κB activation and DNA binding kinetics, as well as causing more rapid degradation of the NF-κB inhibitor, IκBα
PMID: 16920490, 15928677
LPS induces expression of negative regulators of key adaptor/signalling molecules (e.g. IRAK-M and SOCS1 that target IRAKs, ST2L that sequesters MyD88 and MAL) (Liew et al., 2005).
PMID: 16920490, 15928677
LPS induces expression of negative regulators of key adaptor/signalling molecules (e.g. IRAK-M and SOCS1 that target IRAKs, ST2L that sequesters MyD88 and MAL) (Liew et al., 2005).
PMID: 16920490, 9864217
IFNγ pre-treatment of RAW264.7 cells promoted LPS-induced NF-κB activation and DNA binding kinetics, as well as causing more rapid degradation of the NF-κB inhibitor, IκBα (Held et al., 1999)
PMID: 16920490, 11972023, 10975834, 9649436
STAT1 is phosphorylated at both sites following IFNγ exposure; the IFNγ receptor/JAK complex directly mediates Y701 phosphorylation, whereas S727 phosphorylation occurs via a separate pathway involving Ca(2+)/calmodulin-dependent kinase II
PMID: 16920490, 9864217
IFNγ pre-treatment of RAW264.7 cells promoted LPS-induced NF-κB activation and DNA binding kinetics, as well as causing more rapid degradation of the NF-κB inhibitor, IκBα