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PMID: 14643884, 11696589, 9398616, 12385023
There is evidence that LPS stimulation of macrophages or DCs results in PKC activation.</csml:comment>
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IRAK associates with TRAF-6 in the cytoplasm. </csml:comment>
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Binding of RACK to PKC isoforms</csml:comment>
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IRAK is recruited by its DD (grey region)</csml:comment>
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indirect</csml:comment>
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TIRAP exclusively regulates phenotypic maturation of DC: increase of CD40, CD80 and CD86 surface expression. IL-12 p70 is produced only in response to TLR-4 signaling.</csml:comment>
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PMID: 14643884
The TLRs recognize molecular patterns that are characteristic of particular classes of microorganism,
such as lipopolysaccharide (LPS; Gram-negative bacteria), double-stranded RNA (viruses) and mannan (fungi).
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IRAK associates with TRAF-6 in the cytoplasm. 
Subsequently, tumor-necrosis factor receptor (TNFR)-associated factor 6 (TRAF-6) is activated, triggering the NF-_B and mitogen-activated protein kinase (MAPK) pathways, which leads to secretion of pro-inflammatory cytokines (O’Neill, 2002; Takeda, Kaisho, &amp; Akira, 2003)</csml:comment>
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PMID: 14643884, 11937546
initiated upon LPS binding to TLR-4, predominantly leading to nuclear factor NF-kB and mitogen-activated protein (MAP) kinases activation. PKC isoforms actively participate in several TLR signaling pathways.

PMID: 14643884, 11521059
Nevertheless, NF-kB and MAPKs can still be activated by TLR-4 but not TLR-2 in DCs derived from MyD88 −/− mice, supporting the existence of an alternative, MyD88-independent pathway.</csml:comment>
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TIRAP exclusively regulates phenotypic maturation of DC: increase of CD40, CD80 and CD86 surface expression. IL-12 p70 is produced only in response to TLR-4 signaling.
whereas stimulation through TLR-2 with Staphylococcus aureus peptidoglycan (PGN) results only in the release of the IL-12 p40 (Fig. 2) (Re&amp; Strominger, 2001; Nau, Schlesinger, Richmond, &amp; Young, 2003)

c-Rel and NF-_B1/p50 are essential for LPS-induced IL-12 production (Ouaaz, Arron, Zheng, Choi, &amp; Beg, 2002)</csml:comment>
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PMID: 14643884
initiated upon LPS binding to TLR-4, predominantly leading to nuclear factor (NF)-kB and mitogen-activated protein (MAP) kinases activation. PKC isoforms actively participate in several TLR signaling pathways.

PMID: 14643884, 11521059
Nevertheless, NF-kB and MAPKs can still be activated by TLR-4 but not TLR-2 in DCs derived from MyD88 −/− mice, supporting the existence of an alternative, MyD88-independent pathway.</csml:comment>
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TIRAP and MyD88 are recruited to both TLR-4 and TLR-2 by TIR domain interactions
Signaling downstream from certain TLRs, such as TLR-2, appears to be completely dependent on MyD88 (Fig. 2) (Yamamoto et al., 2002).</csml:comment>
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IRAK is recruited by its DD (grey region)</csml:comment>
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TRAF-6 forms a complex with TAB1-TAB2-TAK1 upon which TAK1 mediates downstream NF-_B, p38, ERK and JNK activation. </csml:comment>
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TRAF-6 forms a complex with TAB1-TAB2-TAK1 upon which TAK1 mediates downstream NF-_B, p38, ERK and JNK activation. </csml:comment>
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PMID: 14643884
The TLRs recognize molecular patterns that are characteristic of particular classes of microorganism,
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PMID: 14643884, 11937546
LPS inducible IRAK activation/degradation has been demonstrated to require a functional TLR-4 that can be inhibited by a protein kinase C inhibitor, calphostin</csml:comment>
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PMID: 14643884, 11937546
LPS inducible IRAK activation/degradation has been demonstrated to require a functional TLR-4 that can be inhibited by a protein kinase C inhibitor, calphostin</csml:comment>
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PMID: 14643884
The TLRs recognize molecular patterns that are characteristic of particular classes of microorganism,
such as lipopolysaccharide (LPS; Gram-negative bacteria), double-stranded RNA (viruses) and mannan (fungi).

PMID: 14643884, 11937546
LPS inducible IRAK activation/degradation has been demonstrated to require a functional TLR-4 that can be inhibited by a protein kinase C inhibitor, calphostin.</csml:comment>
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PMID: 14643884
The TLRs recognize molecular patterns that are characteristic of particular classes of microorganism,
such as lipopolysaccharide (LPS; Gram-negative bacteria), double-stranded RNA (viruses) and mannan (fungi).


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The cytoplasmic domains of the TLRs and members of the interleukin-1 receptor (IL-1R) family contain a conserved signal-transduction module— the Toll-interleukin 1 receptor (TIR) domain through which TIR-containing adaptor molecules recruit the putative serine/threonine kinase, IL-1Rassociated kinase (IRAK)</csml:comment>
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TIRAP/MyD88-independent pathway downstream of TLR-4 activates IRF-3 through TICAM-1 which in turn induces INF-beta.</csml:comment>
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TIRAP/MyD88-independent pathway downstream of TLR-4 activates IRF-3 through TICAM-1 which in turn induces INF-beta.

TIR-containing adaptor molecule (TICAM-1), can activate type I IFN-beta gene promoter directly through interferon response factor (IRF)-3 upon TLR-4 triggering</csml:comment>
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