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p(HGNCGENEFAMILY:Caspases)

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Entity

Name
Caspases
Namespace
hgnc.genefamily
Namespace Version
20181015
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/3074b85b858455d8eeb76cfcdef685ced19bbe11/external/hgnc.genefamily-names.belns

Appears in Networks 2

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

In-Edges 6

act(p(HGNC:CHRM1)) decreases act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

Activation of M1 mAChR also protects against apoptotic factors in human neuroblastoma SH-SY5Y cells, such as DNA damage, oxidative stress, caspase activation, and mitochondrial impairment[83]. In addition, apoptosis induced by serum deprivation is blocked by M1 mAChR activation in a phosphoinositide 3-kinase- and MAPK/ERKindependent manner PubMed:24590577

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Experimental Factor Ontology (EFO)
SH-SY5Y

act(a(CHEBI:Thrombin)) increases act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

Thrombin signaling can also activate caspases (36). Proteasomal impairment appears to be upstream of caspase activation, as inhibiting the proteasome with epoxomicin (EPX) led to activation of caspase-3 in primary neurons (63) and in a neuroblastoma cell line expressing wild-type tau (64). PubMed:24027553

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a(MESH:"9-deoxy-delta-9-prostaglandin D2") increases act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553

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path(MESH:"Neurofibrillary Tangles") positiveCorrelation act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

There was a strong correlation between active caspases and the presence of tangles within viable neurons. In the few cells found that were caspase-positive and tangle-negative, 88% had tangles within 24 h (56). This seems to further support a role for caspase cleavage in the evolution of tau pathology. PubMed:24027553

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MeSH
Neurons
Text Location
Review

path(MESH:"Neurofibrillary Tangles") association act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

Furthermore, active caspase co-localizes to NFTs (58), and caspase-cleaved tau is found in AD-affected brain regions, particularly in neurons displaying tangle pathology (59, 60). This includes tau cleaved by caspase-6 in the C-terminus (58–60) as well as in the N-terminus (24). TauC3 is present in AD brain – in neurons and co-localized with NFTs – and inversely correlates with cognitive function (55, 60, 61). PubMed:24027553

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MeSH
Alzheimer Disease
Text Location
Review

path(MESH:Inflammation) association act(p(HGNCGENEFAMILY:Caspases)) View Subject | View Object

First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553

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Text Location
Review

Out-Edges 7

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

Also of importance is understanding the role of non-degradative cleavage in influencing the eventual clearance of tau. Numerous proteases have been shown to proteolyze tau including aminopeptidases (10–12), thrombin (13–15), human high temperature requirement serine protease A1 (HTRA1) (16), calpain (17–20), and caspases (21–24). PubMed:24027553

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

There is significant evidence that tau is a caspase substrate and that caspase-mediated tau cleavage may play a role in AD pathology. Early in vitro studies demonstrated that tau is cleaved in the C-terminus by several caspases including caspase-3 and caspase-6 (21–23). PubMed:24027553

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MeSH
Alzheimer Disease
Text Location
Review

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

First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553

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Text Location
Review

act(p(HGNCGENEFAMILY:Caspases)) positiveCorrelation path(MESH:"Neurofibrillary Tangles") View Subject | View Object

There was a strong correlation between active caspases and the presence of tangles within viable neurons. In the few cells found that were caspase-positive and tangle-negative, 88% had tangles within 24 h (56). This seems to further support a role for caspase cleavage in the evolution of tau pathology. PubMed:24027553

Appears in Networks:
Annotations
MeSH
Neurons
Text Location
Review

act(p(HGNCGENEFAMILY:Caspases)) association path(MESH:"Neurofibrillary Tangles") View Subject | View Object

Furthermore, active caspase co-localizes to NFTs (58), and caspase-cleaved tau is found in AD-affected brain regions, particularly in neurons displaying tangle pathology (59, 60). This includes tau cleaved by caspase-6 in the C-terminus (58–60) as well as in the N-terminus (24). TauC3 is present in AD brain – in neurons and co-localized with NFTs – and inversely correlates with cognitive function (55, 60, 61). PubMed:24027553

Appears in Networks:
Annotations
MeSH
Alzheimer Disease
Text Location
Review

act(p(HGNCGENEFAMILY:Caspases)) association path(MESH:Inflammation) View Subject | View Object

First, inflammation, which is a common feature of AD, may contribute to tau pathology by activating caspases. Treating cells with the prostaglandin cyclopentenone byproduct PGJ2 increased caspase activity and increased cleaved tau (62). PubMed:24027553

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Text Location
Review

act(p(HGNCGENEFAMILY:Caspases)) increases a(HBP:"Tau aggregates") View Subject | View Object

In both studies caspase activation correlated with the appearance and increase over time of caspase-cleaved tau species, which appeared to subsequently form aggregates in the neurons (63). While the mechanism is unclear, a possibility is that accumulating proteins might be a factor in initiating caspase activation. PubMed:24027553

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