Nanopublications LDF server

Matches in Nanopublications for { ?s ?p "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" ?g. }

• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _6 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.
• _5 value "From full text: TLRs signal through two main pathways, defined by the adaptor molecules used at the start of each. The best characterized of these is the MyD88-dependent pathway, common to all TLRs except TLR3, which results in rapid activation of the transcription molecules nuclear factor ?B (NF-?B), activator protein 1 and Elk-1 and induction of proinflammatory mediators such as tumour necrosis factor-? (TNF-?), interleukin-6 (IL-6) and cyclooxygenase-2.13,14 Activation of the NF-?B p65 and activator protein 1 transcription factors is reduced in endotoxin-tolerant cells.15 TLR7, -8 and -9 can also induce type I interferon (IFN) production in a MyD88-dependent manner, involving the activation of the interferon regulatory factor 5 (IRF-5)16 and IRF-717 transcription factors. The second, less well-studied pathway is thought to be limited to TLR3 and TLR4. TLR signalling via the adaptor molecules Toll/IL-1-receptor-domain-containing adaptor inducing IFN-? (TRIF) and TRIF-related adaptor molecule (TRAM) activates IRF-3 and IRF-7 and, ultimately, IFN-inducible genes such as IFN-?-inducible protein 10 (IP-10) and RANTES, via type I IFN production and autocrine activation of the JAK/STAT pathway" provenance.