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Appears in Networks 4

In-Edges 7

a(MESH:"Area Postrema") positiveCorrelation p(HGNC:UCHL1) View Subject | View Object

However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719

a(MESH:"Solitary Nucleus") positiveCorrelation p(HGNC:UCHL1) View Subject | View Object

However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719

act(p(FPLX:PKA)) increases p(HGNC:UCHL1) View Subject | View Object

Activated PKA induces transcription of ApUCH (UCH-L1 in mammals), a deubiquitinating enzyzme, which has been found to be critical for the induction of long-term facilitation (Hegde et al. 1997). PubMed:22908190

path(MESH:"Alzheimer Disease") association p(HGNC:UCHL1) View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

path(MESH:"Parkinson Disease") association p(HGNC:UCHL1) View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

act(p(FPLX:NFkappaB)) decreases p(HGNC:UCHL1) View Subject | View Object

The decrease in Uch-L1 depends on NF-κB pathway since NF-κB p65 can interact with the −300 bp and −109 bp NF-κB binding sequences of the Uch-L1 gene promoter [55]. PubMed:27288790

Out-Edges 14

p(HGNC:UCHL1) decreases bp(GO:"protein ubiquitination") View Subject | View Object

It has been reported recently that while the monomeric form of UCH-L1 catalyzes deubiquitination, the dimers display a ubiquitin ligase activity that generates ubiquitin-K63 bonds (Liu et al., 2002). PubMed:14556719

p(HGNC:UCHL1) increases p(HGNC:SNCA, pmod(Ub)) View Subject | View Object

Mono- and diubiquitinated alphaSYN were polyubiquitinated by the enzyme, suggesting that it acts as an E4 (Koegl et al., 1999) PubMed:14556719

p(HGNC:UCHL1) decreases path(MESH:"Deglutition Disorders") View Subject | View Object

However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719

p(HGNC:UCHL1) positiveCorrelation a(MESH:"Solitary Nucleus") View Subject | View Object

However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719

p(HGNC:UCHL1) positiveCorrelation a(MESH:"Area Postrema") View Subject | View Object

However, mice homozygous for both UCH-L1 and UCH-L3 deletions die early due to dysphagia and display degeneration of the nucleus tractus solitarius and area postrema in addition to the degeneration of the gracile tract that is observed in GAD mice that only have a UCH-L1 deletion PubMed:14556719

p(HGNC:UCHL1) association path(MESH:"Parkinson Disease") View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

p(HGNC:UCHL1) association path(MESH:"Alzheimer Disease") View Subject | View Object

Although UCH-L1 is genetically associated with Parkinson’s disease (i.e., it is the PARK5 gene; Belin and Westerlund 2008), it has also been implicated in the pathogenesis of AD PubMed:22908190

p(HGNC:UCHL1) increases act(a(GO:synapse)) View Subject | View Object

Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190

p(HGNC:UCHL1) increases bp(GO:memory) View Subject | View Object

Moreover, administration of UCH-L1 can reverse the amyloid b-protein–induced synaptic dysfunction and memory loss in transgenic mice overexpressing APP and PS1 (Gong et al. 2006). PubMed:22908190

p(HGNC:UCHL1) decreases p(HGNC:BACE1) View Subject | View Object

Aβ 42 mediated increase in BACE1 expression is accompanied by a decrease in Uch-L1 expression and activity in dif- ferent cellular models and in sporadic AD brains, which interferes with the lysosomal degradation of BACE1 [52,56]. PubMed:27288790

act(p(HGNC:UCHL1)) decreases p(HGNC:BACE1) View Subject | View Object

Aβ 42 mediated increase in BACE1 expression is accompanied by a decrease in Uch-L1 expression and activity in dif- ferent cellular models and in sporadic AD brains, which interferes with the lysosomal degradation of BACE1 [52,56]. PubMed:27288790

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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.