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p(HGNC:SOD1, var("?"))

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Entity

Name
SOD1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 2

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

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

In-Edges 9

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") increases deg(p(HGNC:SOD1, var("?"))) View Subject | View Object

The mutant SOD1 proteins, unlike the wild-type form, are degraded by the UPS (Hoffman et al., 1996;Johnston et al., 2000). PubMed:14556719

Appears in Networks:

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") increases deg(p(HGNC:SOD1, var("?"))) View Subject | View Object

Similarly, overexpression of the putative SOD1 E3 ligase dorfin can inhibit cell death induced by the mutant protein (Niwa et al., 2002), presumably by promoting its removal via the UPS. PubMed:14556719

Appears in Networks:

bp(GO:"proteasome-mediated ubiquitin-dependent protein catabolic process") increases deg(p(HGNC:SOD1, var("?"))) View Subject | View Object

Urushitani and coworkers (Urushitani et al., 2002) showed that mutant SOD1 is degraded by the UPS in cultured cells and that oxidative damage increases the degree of ubiquitination of mutant but not of wild-type SOD1. PubMed:14556719

Appears in Networks:

act(complex(GO:"proteasome complex")) negativeCorrelation p(HGNC:SOD1, var("?")) View Subject | View Object

They found that the proteasome catalytic activity was decreased in neuroblastoma cells following 1 week of expression of a mutant SOD1 gene. PubMed:14556719

Appears in Networks:

composite(a(CHEBI:lactacystin), p(HGNC:SOD1, var("?"))) hasComponent p(HGNC:SOD1, var("?")) View Subject | View Object

Appears in Networks:

p(HGNC:SOD1) hasVariant p(HGNC:SOD1, var("?")) View Subject | View Object

Appears in Networks:

p(HGNC:RNF19A) increases deg(p(HGNC:SOD1, var("?"))) View Subject | View Object

Interestingly, dorfin expression is increased in the spinal cord of ALS patients (Ishigaki et al., 2002), which may suggest that the expression of the E3 ligase is increased in an attempt to enhance clearance of the mutant SOD1. PubMed:14556719

Appears in Networks:

path(MESH:"Amyotrophic Lateral Sclerosis") association p(HGNC:SOD1, var("?")) View Subject | View Object

There is very little evidence to suggest that alterations in SOD are a common feature of sporadic ALS (Alexander et al., 2002). PubMed:14556719

Appears in Networks:

p(HGNC:SQSTM1) association p(HGNC:SOD1, var("?")) View Subject | View Object

p62 localizes to a variety of ubiquitin-positive neuropathological inclusions including Lewy bodies in Parkinson’s disease, neurofibrillary tangles in tauopathies, polyglutamine-expanded huntingtin aggregates in Huntington’s disease, and aggregates of mutant SOD1 in familial amyotrophic lateral sclerosis [85–87]. PubMed:18930136

Appears in Networks:
Annotations
MeSH
Amyotrophic Lateral Sclerosis

Out-Edges 7

p(HGNC:SOD1, var("?")) association path(MESH:"Amyotrophic Lateral Sclerosis") View Subject | View Object

There is very little evidence to suggest that alterations in SOD are a common feature of sporadic ALS (Alexander et al., 2002). PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) increases bp(GO:"response to oxidative stress") View Subject | View Object

The first is that the mutant protein promotes oxidative stress through a gain-of-function mechanism where improper handling of copper may lead to the enzyme catalyzing aberrant pro-oxidant reactions (Cleveland and Liu, 2000). PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) increases bp(GO:"response to oxidative stress") View Subject | View Object

In the other model, the expression of mutant SOD1 alone was sufficient to induce oxidative stress, giving rise to increased proteasome activity, possibly due to the need to remove oxidatively damaged proteins (Hyun et al., 2003). PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) increases bp(GO:"cell death") View Subject | View Object

Similarly, overexpression of the putative SOD1 E3 ligase dorfin can inhibit cell death induced by the mutant protein (Niwa et al., 2002), presumably by promoting its removal via the UPS. PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) negativeCorrelation act(complex(GO:"proteasome complex")) View Subject | View Object

They found that the proteasome catalytic activity was decreased in neuroblastoma cells following 1 week of expression of a mutant SOD1 gene. PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) increases act(complex(GO:"proteasome complex")) View Subject | View Object

In the other model, the expression of mutant SOD1 alone was sufficient to induce oxidative stress, giving rise to increased proteasome activity, possibly due to the need to remove oxidatively damaged proteins (Hyun et al., 2003). PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) association p(HGNC:SQSTM1) View Subject | View Object

p62 localizes to a variety of ubiquitin-positive neuropathological inclusions including Lewy bodies in Parkinson’s disease, neurofibrillary tangles in tauopathies, polyglutamine-expanded huntingtin aggregates in Huntington’s disease, and aggregates of mutant SOD1 in familial amyotrophic lateral sclerosis [85–87]. PubMed:18930136

Appears in Networks:
Annotations
MeSH
Amyotrophic Lateral Sclerosis

About

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.