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a(GO:autolysosome)

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Entity

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

Appears in Networks 4

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

Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

In-Edges 7

p(MGI:Mapt, var("p.Ala152Thr")) increases a(GO:autolysosome) View Subject | View Object

We found that abundance of autophagic vacuoles (autophagosomes + autolysosomes) significantly increased in cells expressing either of the two tau mutants (Fig. 4d,e). This increase was mainly due to higher content of autolysosomes (red puncta) (Fig. 4d,e), in support of increased macroautophagic flux PubMed:29024336

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

p(MGI:Mapt, var("p.Pro301Leu")) increases a(GO:autolysosome) View Subject | View Object

We found that abundance of autophagic vacuoles (autophagosomes + autolysosomes) significantly increased in cells expressing either of the two tau mutants (Fig. 4d,e). This increase was mainly due to higher content of autolysosomes (red puncta) (Fig. 4d,e), in support of increased macroautophagic flux PubMed:29024336

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

path(MESH:"Alzheimer Disease") increases a(GO:autolysosome) View Subject | View Object

Pathologically, the AD brains show both accumulated autophagosomes and autolysosomes, suggesting the basal autophagy process in neurons is abnormal in AD (Fig. 3A). PubMed:23528736

Appears in Networks:
Annotations
MeSH
Brain

bp(GO:"lysosomal protein catabolic process") decreases a(GO:autolysosome) View Subject | View Object

Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300

Appears in Networks:
Annotations
MeSH
Brain

path(MESH:"Alzheimer Disease") positiveCorrelation a(GO:autolysosome) View Subject | View Object

Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300

Appears in Networks:
Annotations
MeSH
Brain

complex(a(GO:amphisome), a(GO:lysosome)) increases a(GO:autolysosome) View Subject | View Object

In mammals, autophagosomes first fuse with endosomes and multivesicular bodies to form amphisomes, which subsequently fuse with lysosomes to create degradative vacuoles termed autolysosomes [17]. PubMed:18930136

Appears in Networks:

path(MESH:"Huntington Disease") positiveCorrelation a(GO:autolysosome) View Subject | View Object

In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136

Appears in Networks:

Out-Edges 3

a(GO:autolysosome) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300

Appears in Networks:
Annotations
MeSH
Brain

a(GO:autolysosome) positiveCorrelation path(MESH:"Huntington Disease") View Subject | View Object

In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136

Appears in Networks:

a(GO:autolysosome) decreases path(HBP:Neurodegeneration) View Subject | View Object

CLN3-related neurodegeneration appears to be a consequence of reduced autophagosome-lysosome fusion [42]. PubMed:18930136

Appears in Networks:

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.