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a(CHEBI:wortmannin)

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Entity

Name
wortmannin
Namespace
chebi
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/chebi-names.belns

Appears in Networks 3

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.0

Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1

In-Edges 4

p(HGNC:MAPT, pmod(Ph, Ser, 262)) positiveCorrelation a(CHEBI:wortmannin) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

p(HGNC:MAPT, pmod(Ph, Ser, 356)) positiveCorrelation a(CHEBI:wortmannin) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

composite(a(CHEBI:wortmannin), p(HGNC:MAPT)) hasComponent a(CHEBI:wortmannin) View Subject | View Object

Appears in Networks:

p(HGNC:MAPT, pmod(Ph, Ser, 262), pmod(Ph, Ser, 356)) positiveCorrelation a(CHEBI:wortmannin) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Dendrites

Out-Edges 10

a(CHEBI:wortmannin) decreases act(a(CHEBI:estrogen)) View Subject | View Object

ApoE-epsilon4, but not ApoE-epsilon3, disrupts carbachol-stimulated phosphoinositol (PI) hydrolysis and so does Abeta and Abeta/ApoE-epsilon4 complexes in SH-SY5Y cells (Cedazo- Mínguez and Cowburn, 2001). The effect of Abeta and its ApoE complex on PI hydrolysis were blocked by estrogen, and this disruption was itself blocked by wortmannin, suggesting that PI3K mediates estrogen’s effect on PI hydrolysis. PubMed:19293145

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:wortmannin) decreases bp(GO:autophagy) View Subject | View Object

In order to determine the impact of protein degradation systems on the sorting of MAPT, we sought to suppress their activity by treating neurons on the neuritic side of the MFCs with either autophagy inhibitors, wortmannin [25] and bafilomycin A 1 [26], or with proteasomal inhibitors, epoxomicin and lactacystin [27,28]. PubMed:30145931

Appears in Networks:

a(CHEBI:wortmannin) increases p(HGNC:MAPT) View Subject | View Object

Compared with the MAPT-free dendrites of control neurons (Fig. S4A, 1.8±0.1), a substantial increase of SQSTM1 level (21.1±0.9) was observed in MAPT-containing dendrites upon wortmannin treatment (Fig. S4B). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:wortmannin) positiveCorrelation p(HGNC:MAPT, pmod(Ph, Ser, 262)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:wortmannin) positiveCorrelation p(HGNC:MAPT, pmod(Ph, Ser, 356)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:wortmannin) causesNoChange p(HGNC:MAPT, pmod(Ph, Ser, 202)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:wortmannin) causesNoChange p(HGNC:MAPT, pmod(Ph, Thr, 205)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:wortmannin) decreases a(MESH:"Dendritic Spines") View Subject | View Object

MAPT-free dendrites in controls had a spine density of ~17 per 20-µm (17.2±0.5 per 20 µm) length, and there was a ~2- fold decrease in spine density in the MAPT-containing dendrites in neurons treated with wortmannin (7.4±1.0 per 20 µm) or epoxomicin (8.2±1.7 per 20 µm) (Fig. 6D). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Neurons

a(CHEBI:wortmannin) positiveCorrelation p(HGNC:MAPT, pmod(Ph, Ser, 262), pmod(Ph, Ser, 356)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Dendrites

a(CHEBI:wortmannin) causesNoChange p(HGNC:MAPT, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205)) View Subject | View Object

Missorted dendritic MAPT showed phosphorylation mainly at the 12E8 sites upon treatment with either the autophagy inhibitor wortmannin (Fig. 4B; 57.2±9.4% dendrites) or the proteasomal inhibitor epoxomicin (Fig. 4C, 62.9±7.4% dendrites) (Fig. 4A-C, quantification in Fig. 4D), but not at the AT8 and the PHF1 (p-S396/p-S404) sites (Fig. S5, Fig 4D). PubMed:30145931

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Dendrites

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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.