Name
Tauopathies
Namespace Keyword
MeSHDisease
Namespace
MeSH
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/mesh-diseases/mesh-diseases-20170511.belanno

Sample Annotated Edges 5

act(p(HGNC:CTSD)) decreases path(HBP:neurotoxicity) View Subject | View Object

Cathepsin D seems particularly important for degrading tau, as its expression was neuroprotective in a Drosophila tauopathy model. Levels of cathepsin D are elevated in flies expressing mutant human tau. If cathepsin D is genetically ablated, these tau flies exhibit enhanced neurotoxicity and a shorter lifespan (93). PubMed:24027553

p(HGNC:CAPN2) positiveCorrelation path(MESH:"Neurofibrillary Tangles") View Subject | View Object

The active form of calpain-2 is found in 50–75% of NFTs in tauopathies including AD, but not in protein aggregates found in other diseases (47). This is consistent with another study that found equivalent calpain levels between control and AD cases, but the activity level of the enzyme isolated from AD brain tissue was increased (48). PubMed:24027553

act(p(HGNC:CTSD)) increases path(MESH:Neuroprotection) View Subject | View Object

Cathepsin D seems particularly important for degrading tau, as its expression was neuroprotective in a Drosophila tauopathy model. Levels of cathepsin D are elevated in flies expressing mutant human tau. If cathepsin D is genetically ablated, these tau flies exhibit enhanced neurotoxicity and a shorter lifespan (93). PubMed:24027553

act(p(HGNC:CTSD)) increases deg(p(HGNC:MAPT)) View Subject | View Object

Cathepsin D seems particularly important for degrading tau, as its expression was neuroprotective in a Drosophila tauopathy model. Levels of cathepsin D are elevated in flies expressing mutant human tau. If cathepsin D is genetically ablated, these tau flies exhibit enhanced neurotoxicity and a shorter lifespan (93). PubMed:24027553

act(p(HGNCGENEFAMILY:Calpains)) increases path(HBP:Neurodegeneration) View Subject | View Object

On the one hand, expressing a 17-kDa fragment of tau based on calpain cleavage site mapping in hippocampal neurons led to neurite retraction and the appearance of varicosities after 48 h (52). Additionally, suppressing calpain activity in a fly model of tauopathy prevented neurodegeneration, as did expressing a calpain-resistant form of tau (54). PubMed:24027553

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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.