Sandbox GGC12: Difference between revisions

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== Function ==

Controls the host immune response system against any pathogens through the recognition of molecular patterns tahat are specific to each microorganism. TLR3 is a nuclear-sensing TLR which is going to be activated by double-stranded RNA, a sign of viral infection. Acts via the adapter TRIF/TICAM1, ~~leading~~ to NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response <ref>PMID:12471095</ref>.

Controls the host immune response system against any pathogens through the recognition of molecular patterns tahat are specific to each microorganism. TLR3 is a nuclear-sensing TLR which is going to be essentially activated by a double-stranded RNA, which is a sign of a viral infection. Acts via the adapter TRIF/TICAM1, that leads to a NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response <ref>PMID:12471095</ref>.

== Disease ==

A rare complication of human herpesvirus 1 (HHV-1) infection, ~~occurring~~ in only small ~~minorities~~ of HHV-1 infected individuals. ~~It is~~ characterized by hemorrhagic necrosis of parts of the temporal and frontal lobes. ~~Onset is over~~ several days ~~and involves~~ fear, headache, seizures, stupor, and often coma, frequently with a fatal outcome <ref>PMID:17872438</ref>.

A rare complication of human herpesvirus 1 (HHV-1) infection, it occurs in only a small minority of HHV-1 infected individuals. There are characterized by a hemorrhagic necrosis of parts from both the temporal and frontal lobes. One of the onsets are that it invloves several days of fear, headache, seizures, stupor, and often coma, frequently with a fatal outcome <ref>PMID:17872438</ref>.

== Relevance ==

TRIF pathway

Various pathogens target the signaling molecules and transcriptional regulators acting in the TRIF pathway, ~~thus demonstrating~~ the importance of this pathway contributes to control of both viral and bacterial pathogens through promotion of inflammatory mediators and ~~activator~~ of antimicrobial responses. TRIF signaling also has both protective and pathologic roles in several chronic inflammatory disease conditions, as well as an essential function in wound‐repair processes <ref>DOI 10.1189/jlb.2RI1115-531R</ref>.

Various of the pathogens do target the signaling molecules and transcriptional regulators which are acting in the TRIF pathway, it goes on to demonstrate the main importance of this particular pathway which contributes to control of both viral and bacterial pathogens through a promotion of the inflammatory mediators and activators of antimicrobial responses. TRIF signaling also has both protective and pathologic roles in several chronic inflammatory disease conditions, as well as an essential function in wound‐repair processes <ref>DOI 10.1189/jlb.2RI1115-531R</ref>.

TICAM1

Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively. Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens. Component of a multi-helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of proinflammatory cytokines. Ubiquitously expressed but with higher levels in liver.

Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively. Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens. Component of a multi-helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of proinflammatory cytokines. Ubiquitously expressed but with higher levels in liver <ref>DOI 10.1016/j.jmb.2013.11.024</ref>.

IRF3

Sandbox GGC12: Difference between revisions

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@@ Line 5: / Line 5: @@
 == Function ==
-Controls the host immune response system against any pathogens through the recognition of molecular patterns tahat are specific to each microorganism. TLR3 is a nuclear-sensing TLR which is going to be activated by double-stranded RNA, a sign of viral infection. Acts via the adapter TRIF/TICAM1, leading to NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response <ref>PMID:12471095</ref>.
+Controls the host immune response system against any pathogens through the recognition of molecular patterns tahat are specific to each microorganism. TLR3 is a nuclear-sensing TLR which is going to be essentially activated by a double-stranded RNA, which is a sign of a viral infection. Acts via the adapter TRIF/TICAM1, that leads to a NF-kappa-B activation, IRF3 nuclear translocation, cytokine secretion and the inflammatory response <ref>PMID:12471095</ref>.
 == Disease ==
-A rare complication of human herpesvirus 1 (HHV-1) infection, occurring in only small minorities of HHV-1 infected individuals. It is characterized by hemorrhagic necrosis of parts of the temporal and frontal lobes. Onset is over several days and involves fear, headache, seizures, stupor, and often coma, frequently with a fatal outcome <ref>PMID:17872438</ref>.
+A rare complication of human herpesvirus 1 (HHV-1) infection, it occurs in only a small minority of HHV-1 infected individuals. There are characterized by a hemorrhagic necrosis of parts from both the temporal and frontal lobes. One of the onsets are that it invloves several days of fear, headache, seizures, stupor, and often coma, frequently with a fatal outcome <ref>PMID:17872438</ref>.
 == Relevance ==
 TRIF pathway
-Various pathogens target the signaling molecules and transcriptional regulators acting in the TRIF pathway, thus demonstrating the importance of this pathway contributes to control of both viral and bacterial pathogens through promotion of inflammatory mediators and activator of antimicrobial responses. TRIF signaling also has both protective and pathologic roles in several chronic inflammatory disease conditions, as well as an essential function in wound‐repair processes <ref>DOI 10.1189/jlb.2RI1115-531R</ref>.
+Various of the pathogens do target the signaling molecules and transcriptional regulators which are acting in the TRIF pathway, it goes on to demonstrate the main importance of this particular pathway which contributes to control of both viral and bacterial pathogens through a promotion of the inflammatory mediators and activators of antimicrobial responses. TRIF signaling also has both protective and pathologic roles in several chronic inflammatory disease conditions, as well as an essential function in wound‐repair processes <ref>DOI 10.1189/jlb.2RI1115-531R</ref>.
 TICAM1
-Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively. Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens. Component of a multi-helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of proinflammatory cytokines. Ubiquitously expressed but with higher levels in liver.
+Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively. Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens. Component of a multi-helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of proinflammatory cytokines. Ubiquitously expressed but with higher levels in liver <ref>DOI 10.1016/j.jmb.2013.11.024</ref>.
 IRF3