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Appears in Networks 1

In-Edges 6

a(CHEBI:"amyloid-beta") increases p(HGNC:MAPT, frag("?", "17kD")) View Subject | View Object

Also, treating primary hippocampal neurons with pre-aggregated amyloid beta (Abeta) led to the generation of tau fragments of ∼35, ∼24, and ∼17 kDa, which was blocked by addition of a calpain inhibitor (52, 53). Tau fragments of the same size were also found in AD brain tissue (19). PubMed:24027553

a(CHEBI:"calpain inhibitor") decreases p(HGNC:MAPT, frag("?", "17kD")) View Subject | View Object

Also, treating primary hippocampal neurons with pre-aggregated amyloid beta (Abeta) led to the generation of tau fragments of ∼35, ∼24, and ∼17 kDa, which was blocked by addition of a calpain inhibitor (52, 53). Tau fragments of the same size were also found in AD brain tissue (19). PubMed:24027553

bp(GO:"apoptotic process") association p(HGNC:MAPT, frag("?", "17kD")) View Subject | View Object

Increasing intracellular calcium levels in PC12 cells leads to calpain-induced cleavage of tau (18). This may reflect a potential effect of excitotoxicity in AD. Inducing apoptosis in cerebellar granule cells yields calpain-mediated tau fragments, including a dominant ∼17 kDa fragment (17). PubMed:24027553

Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

act(p(HGNCGENEFAMILY:Calpains)) increases p(HGNC:MAPT, frag("?", "17kD")) View Subject | View Object

Excitotoxicity leading to elevated intracellular calcium is a common feature of neurodegenerative diseases, and is implicated in AD (49, 50). This process may lead to enhanced activation of calpains (51). This in turn could influence a number of pathologic processes, including tau proteolysis. Indeed, tau has a number of putative calpain cleavage sites, and incubation of recombinant tau with calpain generates specific fragments, including one that is ∼35 kDa and one that is ∼17 kDa (19, 20). PubMed:24027553

act(p(HGNCGENEFAMILY:Calpains)) increases p(HGNC:MAPT, frag("?", "17kD")) View Subject | View Object

Increasing intracellular calcium levels in PC12 cells leads to calpain-induced cleavage of tau (18). This may reflect a potential effect of excitotoxicity in AD. Inducing apoptosis in cerebellar granule cells yields calpain-mediated tau fragments, including a dominant ∼17 kDa fragment (17). PubMed:24027553

Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

Out-Edges 3

p(HGNC:MAPT, frag("?", "17kD")) association bp(GO:"apoptotic process") View Subject | View Object

Increasing intracellular calcium levels in PC12 cells leads to calpain-induced cleavage of tau (18). This may reflect a potential effect of excitotoxicity in AD. Inducing apoptosis in cerebellar granule cells yields calpain-mediated tau fragments, including a dominant ∼17 kDa fragment (17). PubMed:24027553

Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

p(HGNC:MAPT, frag("?", "17kD")) increases bp(HBP:"neurite retraction") 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

p(HGNC:MAPT, frag("?", "17kD")) causesNoChange path(HBP:neurotoxicity) View Subject | View Object

In contrast, another study used mass spectroscopy and sequencing to identify the “17 kDa” tau cleavage product and found it did not correspond to the recombinant fragment utilized in the above studies (19). Expression of a recombinant form of the mass spectroscopy-identified fragment in hippocampal neurons was not toxic (19). 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.