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Results
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Text Location
Namespace Version
1.0.1
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/text-location/text-location-1.0.1.belanno

Sample Annotated Edges 5

a(CHEBI:LY294002) decreases p(HGNC:MAPT, pmod(Ph, Thr, 231)) View Subject | View Object

Interestingly, we found that tau hyperphosphorylation at Thr231 was completely blocked by the Src family tyrosine kinase inhibitor, 4-amino-5-(4- chlorophenyl)-7(t-butyl)pyrazol(3,4-d)pyramide (PP1), and by the phosphatidylinositol 3-kinase inhibitor, LY294002 (Fig. 5). PubMed:17403556

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a(CHEBI:LY294002) decreases bp(GO:"signal transduction") View Subject | View Object

Inhibition occurred even though ADDLs were still bound to cell surfaces, indicating that those kinases are involved in signal transduction coupling between ADDL binding and tau hyperphosphorylation. PubMed:17403556

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a(CHEBI:LY294002) decreases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation)) View Subject | View Object

Moreover, the presence of large extracellular aggregates in NU1-treated cultures (Fig. 5N) suggests that the antibody effectively sequesters ADDLs and prevents their interactions with neurons (Fig. 5O). No inhibition of ADDL binding was associated with PP1 and LY294002 (Fig. 5H, I, K and L, respectively), but both kinase inhibitors effectively blocked ADDL-induced tau hyperphosphorylation (Fig. 5G and J). PubMed:17403556

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a(HBP:"amyloid-beta antibody, NU1") decreases act(a(HBP:"amyloid-beta derived diffusible ligands")) View Subject | View Object

NU1 completely blocked the increase in P-Ser404 and P-Thr231 phosphotau levels induced by ADDLs (Fig. 3D–H). PubMed:17403556

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a(HBP:"amyloid-beta antibody, NU1") decreases complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) View Subject | View Object

Moreover, the presence of large extracellular aggregates in NU1-treated cultures (Fig. 5N) suggests that the antibody effectively sequesters ADDLs and prevents their interactions with neurons (Fig. 5O). No inhibition of ADDL binding was associated with PP1 and LY294002 (Fig. 5H, I, K and L, respectively), but both kinase inhibitors effectively blocked ADDL-induced tau hyperphosphorylation (Fig. 5G and J). PubMed:17403556

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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.