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bp(GO:"late endosomal microautophagy")

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Entity

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

Appears in Networks 1

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

In-Edges 6

a(HBP:HBP00055) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

Absence of the second N-terminal insert also significantly reduced e-MI of tau (Fig. 5e,f) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(MGI:Mapt) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

In the presence of any of the tau proteins, we found some sequestration of the probe in the multivesicular bodies, albeit significantly less in cells expressing the WT and A152T protein PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Ala152Thr")) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

Contrary to WT tau, which accumulates in e- MI-defective cells, intracellular levels of A152T and P301L tau did not change in cells knocked down for Vps4, suggesting that both point mutations in tau compromise its ability to undergo degradation by this pathway (Fig. 2a,b) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Ala152Thr")) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

In the presence of any of the tau proteins, we found some sequestration of the probe in the multivesicular bodies, albeit significantly less in cells expressing the WT and A152T protein PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

p(MGI:Mapt, var("p.Pro301Leu")) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

Contrary to WT tau, which accumulates in e- MI-defective cells, intracellular levels of A152T and P301L tau did not change in cells knocked down for Vps4, suggesting that both point mutations in tau compromise its ability to undergo degradation by this pathway (Fig. 2a,b) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

composite(a(CHEBI:"ammonium chloride"), a(CHEBI:leupeptin)) decreases bp(GO:"late endosomal microautophagy") View Subject | View Object

As expected, fluorescence puncta were visible in transduced control cells (Fig. 4a) and blockage of endo/lysosomal degradation with ammonium chloride and leupeptin significantly increased the number of fluorescent puncta by preventing their degradation (Fig. 4b) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Intracellular Space
Confidence
High
MeSH
Brain

Out-Edges 3

bp(GO:"late endosomal microautophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

In this study, we analyzed the contribution of three different types of autophagy, macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy to the degradation of tau protein variants and tau mutations associated with this agerelated disease. We have found that the pathogenic P301L mutation inhibits degradation of tau by any of the three autophagic pathways, whereas the risk-associated tau mutation A152T reroutes tau for degradation through a different autophagy pathway PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

bp(GO:"late endosomal microautophagy") increases deg(p(MGI:Mapt)) View Subject | View Object

Interestingly, although judging by the studies in intact cells the contribution of e-MI to tau degradation is small (Fig. 2a), our in vitro studies with isolated LE revealed a high efficiency for e-MI of tau (Fig. 2c) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Multivesicular Bodies
Confidence
High
MeSH
Brain

bp(GO:"late endosomal microautophagy") increases deg(a(HBP:HBP00053)) View Subject | View Object

Contrary to WT tau, which accumulates in e- MI-defective cells, intracellular levels of A152T and P301L tau did not change in cells knocked down for Vps4, suggesting that both point mutations in tau compromise its ability to undergo degradation by this pathway (Fig. 2a,b) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

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.