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Entity

Name
Tlr4
Namespace
MGI
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mgi-mouse-genes/mgi-mouse-genes-20170725.belns

Appears in Networks 2

In-Edges 5

p(MGI:Mapt, var("p.Pro301Leu")) increases p(MGI:Tlr4) View Subject | View Object

Consistent with the transcriptomic profile in human NFT-bearing neurons and mouse brain tissue (Figure 1a-c), SASP genes were found to be upregulated in tauNFT brains, i.e., Il1b was 4- and 2-fold higher than CTL and tauWT, respectively; and Cxcl1 was 4-fold higher than both control genotypes; Tnfa was 13- and 8-fold higher than CTL and tauWT, respectively; Tlr4 was 3-fold higher than both control genotypes (Figure 2a-d) PubMed:30126037

p(MGI:Hpx) negativeCorrelation act(p(MGI:Tlr4)) View Subject | View Object

Importantly, by scavenging free heme, Hx prevents heme-induced M1 macrophage polarization and thus avoids both TLR4 activation and ROS formation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(MGI:Hpx) decreases p(MGI:Tlr4) View Subject | View Object

The mechanism postulated for the beneficial effects 398 of hemopexin in mouse models of chronic hemolysis involves inhibition of heme399 dependent activation of TLR4 signaling and a combination of reduced endothelial 400 formation of reactive oxygen species and restored endothelial NOS-activity. PubMed:28314763

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Arteries
MeSH
Diabetes Mellitus
Text Location
Introduction

path(MESH:"Lung Injury") negativeCorrelation act(p(MGI:Tlr4)) View Subject | View Object

These data demonstrate that TLR4 signaling plays a role in heme-induced exacerbation of lung bacterial infection secondary to TH followed by massive resuscitation with stored RBCs. PubMed:29522519

Appears in Networks:
Annotations
Text Location
Results

Out-Edges 5

act(p(MGI:Tlr4)) negativeCorrelation p(MGI:Hpx) View Subject | View Object

Importantly, by scavenging free heme, Hx prevents heme-induced M1 macrophage polarization and thus avoids both TLR4 activation and ROS formation. PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Discussion

p(MGI:Tlr4) increases p(MGI:Vcam1) View Subject | View Object

TLR4 401 activation by free heme would induce mobilization of P-selectin and von Willebrand 402 factor to the endothelial surface that triggers VCAM-1, ICAM-1, and E-selectin403 dependent hemostasis and vasoocclusion (3, 4). PubMed:28314763

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Arteries
MeSH
Diabetes Mellitus
Text Location
Introduction

p(MGI:Tlr4) increases p(MGI:Icam1) View Subject | View Object

TLR4 401 activation by free heme would induce mobilization of P-selectin and von Willebrand 402 factor to the endothelial surface that triggers VCAM-1, ICAM-1, and E-selectin403 dependent hemostasis and vasoocclusion (3, 4). PubMed:28314763

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Arteries
MeSH
Diabetes Mellitus
Text Location
Introduction

p(MGI:Tlr4) increases p(MGI:Sele) View Subject | View Object

TLR4 401 activation by free heme would induce mobilization of P-selectin and von Willebrand 402 factor to the endothelial surface that triggers VCAM-1, ICAM-1, and E-selectin403 dependent hemostasis and vasoocclusion (3, 4). PubMed:28314763

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Arteries
MeSH
Diabetes Mellitus
Text Location
Introduction

act(p(MGI:Tlr4)) negativeCorrelation path(MESH:"Lung Injury") View Subject | View Object

These data demonstrate that TLR4 signaling plays a role in heme-induced exacerbation of lung bacterial infection secondary to TH followed by massive resuscitation with stored RBCs. PubMed:29522519

Appears in Networks:
Annotations
Text Location
Results

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.