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a(CHEBI:epoxomicin)

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Entity

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

Appears in Networks 4

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. 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:epoxomicin) 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:epoxomicin) 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:epoxomicin), p(HGNC:MAPT)) hasComponent a(CHEBI:epoxomicin) View Subject | View Object

Appears in Networks:

p(HGNC:MAPT, pmod(Ph, Ser, 262), pmod(Ph, Ser, 356)) positiveCorrelation a(CHEBI:epoxomicin) 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 14

a(CHEBI:epoxomicin) increases act(p(HGNC:CASP3)) View Subject | View Object

Thrombin signaling can also activate caspases (36). Proteasomal impairment appears to be upstream of caspase activation, as inhibiting the proteasome with epoxomicin (EPX) led to activation of caspase-3 in primary neurons (63) and in a neuroblastoma cell line expressing wild-type tau (64). PubMed:24027553

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:epoxomicin) decreases deg(p(HGNC:MAPT)) View Subject | View Object

Similarly, overexpressing the FTDP-17 mutant P301L tau in SH-SY5Y cells and then treating with lactacystin led to significantly increased tau levels (70). Lactacystin also caused accumulation of endogenous tau in the HT22 murine neuronal cell line (71). In immortalized mouse cortical neuronal cells inducibly expressing full-length wild-type tau, EPX slowed the degradation of full-length tau (72). PubMed:24027553

Appears in Networks:
Annotations
Text Location
Review

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

In M1C neuroblastoma cells that inducibly express wild-type full-length tau (4R0N), EPX, and MG-132 induced accumulation of full-length tau but there was a concomitant loss of C-terminus immunoreactivity (64). PubMed:24027553

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:epoxomicin) decreases act(p(FPLX:Proteasome)) View Subject | View Object

Related to these data, reversible and irreversible proteasome inhibitors including lactacystin, leupeptin, and epoxomicin delay the degradation of endogenous and/or transiently overexpressed tau (Cardozo and Michaud, 2002; David et al., 2002; Zhang et al., 2005). PubMed:23528736

Appears in Networks:

a(CHEBI:epoxomicin) decreases deg(p(HGNC:MAPT)) View Subject | View Object

Related to these data, reversible and irreversible proteasome inhibitors including lactacystin, leupeptin, and epoxomicin delay the degradation of endogenous and/or transiently overexpressed tau (Cardozo and Michaud, 2002; David et al., 2002; Zhang et al., 2005). PubMed:23528736

Appears in Networks:

a(CHEBI:epoxomicin) decreases act(p(FPLX:Proteasome)) 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:epoxomicin) increases bp(GO:"protein ubiquitination") View Subject | View Object

Similarly, a dramatic elevation of ubiquitinated substrates (from 4.2±0.1 to 37±1) upon epoxomicin treatment was detected in dendrites containing MAPT (compare Fig. S4E and Fig. S4F). PubMed:30145931

Appears in Networks:
Annotations
MeSH
Dendrites

a(CHEBI:epoxomicin) 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:epoxomicin) 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:epoxomicin) 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:epoxomicin) 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:epoxomicin) 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:epoxomicin) 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:epoxomicin) 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.