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bp(GO:"autophagosome assembly")

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Entity

Name
autophagosome assembly
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 3

The Biology of Proteostasis in Aging and Disease v1.0.0

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0

In-Edges 10

p(HGNC:RAB1A) increases bp(GO:"autophagosome assembly") View Subject | View Object

In contrast, α-synuclein overexpression impairs autophagy in mammalian cells and mice through reduced expression of RAB1A, thereby inhibiting autophagosome formation (88). PubMed:25784053

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 42") decreases bp(GO:"autophagosome assembly") View Subject | View Object

Sixth, Aβ42 compro- mises the function of AMPK to impede initiation of the ALN 67 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:resveratrol) increases bp(GO:"autophagosome assembly") View Subject | View Object

The multi-modal agent resveratrol induced the expression of ATG4 and promoted autophagosome formation. PubMed:30116051

Appears in Networks:
Annotations
MeSH
Machado-Joseph Disease

a(CHEBI:selenomethionine) increases bp(GO:"autophagosome assembly") View Subject | View Object

Selenium deficits have been linked to AD, and thus it is interesting that seleno- methionine boosted ALN flux, from AMPK recruit- ment through autophagosome formation to lysosomal degradation, in the 3×Tg AD mouse model 112 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

act(p(HGNC:BECN1)) increases bp(GO:"autophagosome assembly") View Subject | View Object

Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051

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act(p(HGNC:AMBRA1)) increases bp(GO:"autophagosome assembly") View Subject | View Object

Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051

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p(HGNC:HTT, var("?")) decreases bp(GO:"autophagosome assembly") View Subject | View Object

Mutant Htt is cleared by autophagy, but it compromises the ALN because of decreased cargo load- ing and impaired autophagosome formation and trans- port 55,56,68,92 . PubMed:30116051

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Annotations
MeSH
Dopaminergic Neurons
MeSH
Huntington Disease

p(HGNC:SNCA, var("?")) decreases bp(GO:"autophagosome assembly") View Subject | View Object

Third, α-synuclein mutations, triplications or excesses amplify the ALN burden, interfere with auto phagosome formation and irreversibly disrupt the lysosomal mem- brane 1,3,44,56 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Parkinson Disease

act(p(HGNC:ULK1)) increases bp(GO:"autophagosome assembly") View Subject | View Object

Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051

Appears in Networks:

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

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Out-Edges 0

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.