1. Catalog
  2. Nodes
  3. a(HBP:HBP00053)

a(HBP:HBP00053)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
HBP00053
Namespace
HBP
Namespace Version
20181029
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/785431732a26d6809b4162d98b95687d16404e63/export/hbp.belns

Appears in Networks 1

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

In-Edges 6

a(GO:lysosome) increases deg(a(HBP:HBP00053)) View Subject | View Object

In agreement with our previous observations (Wang et al., 2009), we found that lysosomes contribute to degradation of WT tau (reflected as an increase in tau levels upon blockage of lysosomal proteolysis with inhibitors) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

bp(GO:"chaperone-mediated autophagy") increases deg(a(HBP:HBP00053)) View Subject | View Object

This lysosomal degradation occurred, in large part, through CMA, as genetic blockage of this pathway almost completely abolished lysosomal degradation of WT tau and led to its accumulation (Fig. 1a,b; GAPDH is shown as an example of a well-characterized CMA substrate (Aniento et al., 1993) known to accumulate intracellularly upon blockage of CMA (Schneider et al., 2014)) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
High
MeSH
Brain

bp(GO:"chaperone-mediated autophagy") increases deg(a(HBP:HBP00053)) View Subject | View Object

Consistent with our previous findings (Wang et al., 2009), WT tau is a very efficient CMA substrate, to the point that binding is almost undetectable because the protein is rapidly internalized (Fig. 1c,d) PubMed:29024336

Appears in Networks:
Annotations
MeSH
Lysosomes
Confidence
Medium
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

composite(a(CHEBI:paraquat), a(HBP:HBP00053)) hasComponent a(HBP:HBP00053) View Subject | View Object

Appears in Networks:

composite(a(CHEBI:thapsigargin), a(HBP:HBP00053)) hasComponent a(HBP:HBP00053) View Subject | View Object

Appears in Networks:

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.