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p(HGNC:UCHL1)

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Entity

Name
UCHL1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

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

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

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

Appears in Networks:

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

Appears in Networks:

complex(p(HGNC:UCHL1), p(HGNC:UCHL1)) hasComponent p(HGNC:UCHL1) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

Out-Edges 14

p(HGNC:UCHL1) hasVariant p(HGNC:UCHL1, var("?")) View Subject | View Object

Appears in Networks:

p(HGNC:UCHL1) hasVariant p(HGNC:UCHL1, var("p.Ile93Met")) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

p(HGNC:UCHL1) hasVariant p(HGNC:UCHL1, pmod(GO:"protein oxidation")) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

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

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

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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.