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Appears in Networks 4

In-Edges 7

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

Annotations
Cell Ontology (CL)
motor neuron

p(HGNC:SOD1, var("p.Gly576Arg")) decreases 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

Annotations
Cell Ontology (CL)
motor neuron

a(CHEBI:"methylene blue") increases p(HGNC:MAP1LC3A) View Subject | View Object

Other compounds that act through AMPK acti- vation include the antiaggregant methylene blue (Supplementary Box 1), which elevated levels of beclin  1, p62 and LC3, induced autophagy and suppressed tau in organotypic neuronal cultures and a mouse model of FTD 101,102 . PubMed:30116051

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

Cilostazol (a phosphodiesterase 3 inhibitor) clears Aβ42 from neuronal cell lines by promoting autophagy, upregulating beclin 1, ATG5 and LC3, downregulating mTORC1 and inducing lysosomal cathepsin B; these actions of cilostazol involve activation of SIRT1 as well as upstream Tyr172 phosphorylation of AMPK 108,162,163 . PubMed:30116051

act(p(HGNC:SIRT1)) increases act(p(HGNC:MAP1LC3A)) View Subject | View Object

SIRT1 is activated by AMPK- mediated increases in nicotinamide, and it drives the ALN by inhibiting mTORC1, inducing FOXO1 and FOXO3 and activating key regulatory proteins such as ATG5, ATG7 and LC3. PubMed:30116051

path(MESH:"Plaque, Amyloid") positiveCorrelation p(HGNC:MAP1LC3A) View Subject | View Object

In these transgenic mice LC3-positive bodies were particularly apparent in neurites surrounding amyloid plaques, and immunoblotting of hippocampi from 6 month old transgenic PS1/APP mice revealed increased levels of LC3-II compared to wild-type mice (81) PubMed:24027553

Out-Edges 3

p(HGNC:MAP1LC3A) positiveCorrelation path(MESH:"Plaque, Amyloid") View Subject | View Object

In these transgenic mice LC3-positive bodies were particularly apparent in neurites surrounding amyloid plaques, and immunoblotting of hippocampi from 6 month old transgenic PS1/APP mice revealed increased levels of LC3-II compared to wild-type mice (81) PubMed:24027553

p(HGNC:MAP1LC3A) increases bp(GO:"autophagosome assembly") View Subject | View Object

ADNP is an essential protein for brain development and it has been shown to physically interact with a key protein in autophagosome biogenesis and maturation, namely LC3 PubMed:30061532

p(HGNC:MAP1LC3A) increases bp(GO:"autophagosome maturation") View Subject | View Object

ADNP is an essential protein for brain development and it has been shown to physically interact with a key protein in autophagosome biogenesis and maturation, namely LC3 PubMed:30061532

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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.