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a(CHEBI:chloroquine)

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Entity

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

Appears in Networks 2

The Biology of Proteostasis in Aging and Disease v1.0.0

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

In-Edges 0

Out-Edges 6

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

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

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Cell Ontology (CL)
motor neuron

a(CHEBI:chloroquine) increases a(CHEBI:"N-retinylidene-N-retinylethanolamine") View Subject | View Object

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

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Annotations
Cell Ontology (CL)
motor neuron

a(CHEBI:chloroquine) increases p(HGNC:MAP1LC3A) View Subject | View Object

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

a(CHEBI:chloroquine) increases p(HGNC:SQSTM1) View Subject | View Object

Reduced levels of lipofuscin, LC3, and p62 have been observed in motor neurons of SOD1(G85R) mice (92). Treatment with the autophagy inhibitor chloroquine restored lipofuscin, LC3, and p62 levels in motor neurons, suggesting that mutant SOD1 causes hyperactive autophagy in mice (92). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

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

Treating hippocampal slices with chloroquine (CQ), which raises the pH of lysosomes to impair enzymatic function, was associated with increased levels of full-length tau (89, 91). PubMed:24027553

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MeSH
Hippocampus
Text Location
Review

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

In M1C neuroblastoma cells that inducibly express full-length wild-type tau (4R0N), treatment with CQ also significantly slowed down tau degradation, and caused its accumulation (92). Treatment of hippocampal slices with the cathepsin modulator ZPAD (which stimulates cathepsin D very strongly) appears to increase the proteolysis of full-length tau resulting in the production of smaller fragments, including a phosphorylated 29 kDa fragment (86, 89). This partial degradation of tau was inhibited by inclusion of a selective cathepsin D inhibitor (86). PubMed:24027553

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Text Location
Review

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.