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Entity

Name
TRIF-dependent toll-like receptor 4 signaling pathway
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 1

In-Edges 2

a(CHEBI:"LPS with O-antigen") increases bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") View Subject | View Object

One checkpoint is that bacterial mRNA from live bacteria (also known as vita-PAMPs)44 activates NLRP3; the other checkpoint is that TLR4- and TRIF (TIR domain-containing adaptor protein inducing IFNβ)-dependent signalling — which is triggered by bacterial lipopolysaccharide (LPS) — mediate the secretion of type I IFNs, inducing pro-caspase 11 expression and activation by triggering the IFNα/β receptor (IFNAR) (FIG. 1). PubMed:23702978

a(CHEBI:cycloheximide) increases bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") View Subject | View Object

In the presence of the translation inhibitor cycloheximide, TRIF signalling that is downstream of TLR3 or TLR4 leads to pro-IL-1β processing by caspase 8 (REF. 55). PubMed:23702978

Out-Edges 4

bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") regulates sec(a(MESH:"Interferon Type I")) View Subject | View Object

One checkpoint is that bacterial mRNA from live bacteria (also known as vita-PAMPs)44 activates NLRP3; the other checkpoint is that TLR4- and TRIF (TIR domain-containing adaptor protein inducing IFNβ)-dependent signalling — which is triggered by bacterial lipopolysaccharide (LPS) — mediate the secretion of type I IFNs, inducing pro-caspase 11 expression and activation by triggering the IFNα/β receptor (IFNAR) (FIG. 1). PubMed:23702978

bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") increases p(HGNC:SCAF11) View Subject | View Object

One checkpoint is that bacterial mRNA from live bacteria (also known as vita-PAMPs)44 activates NLRP3; the other checkpoint is that TLR4- and TRIF (TIR domain-containing adaptor protein inducing IFNβ)-dependent signalling — which is triggered by bacterial lipopolysaccharide (LPS) — mediate the secretion of type I IFNs, inducing pro-caspase 11 expression and activation by triggering the IFNα/β receptor (IFNAR) (FIG. 1). PubMed:23702978

bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") increases act(p(HGNC:IFNAR1)) View Subject | View Object

One checkpoint is that bacterial mRNA from live bacteria (also known as vita-PAMPs)44 activates NLRP3; the other checkpoint is that TLR4- and TRIF (TIR domain-containing adaptor protein inducing IFNβ)-dependent signalling — which is triggered by bacterial lipopolysaccharide (LPS) — mediate the secretion of type I IFNs, inducing pro-caspase 11 expression and activation by triggering the IFNα/β receptor (IFNAR) (FIG. 1). PubMed:23702978

bp(GO:"TRIF-dependent toll-like receptor 4 signaling pathway") increases act(p(HGNC:CASP8)) View Subject | View Object

In the presence of the translation inhibitor cycloheximide, TRIF signalling that is downstream of TLR3 or TLR4 leads to pro-IL-1β processing by caspase 8 (REF. 55). PubMed:23702978

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.