1. Catalog
  2. Nodes
  3. p(HGNC:SOD1)

p(HGNC:SOD1)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

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

Appears in Networks 8

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

The Biology of Proteostasis in Aging and Disease v1.0.0

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

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

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Protein aggregation can inhibit clathrin-mediated endocytosis by chaperone competition v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 9

a(CHEBI:"lithium(1+)") decreases p(HGNC:SOD1) View Subject | View Object

This mechanism may be involved in its promotion of autophagy, reduction in cel- lular levels of α-synuclein, SOD1, Htt and tau 126 , ame- lioration of motor function in a P301L mouse model of tauopathy 127 and slowing of disease progression in SOD1 mice 128 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

complex(p(HGNC:BIRC2), p(HGNC:SOD1)) hasComponent p(HGNC:SOD1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:BIRC2), p(HGNC:SOD1)) increases deg(p(HGNC:SOD1)) View Subject | View Object

Third, cellular inhibitor of apoptosis 1 (CIAP1; also known as BIRC2) specifically binds mutant SOD1 and drives it to proteasomal degradation. PubMed:30116051

Appears in Networks:

p(HGNC:CAST) increases deg(p(HGNC:SOD1)) View Subject | View Object

Calpain inhibition by cal- pastatin or pharmacological agents also confers neuropro- tective effects in other NDA models, including improved clearance of tau, α-synuclein and SOD1 (REFS54,106,107) . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Dopaminergic Neurons

a(PUBCHEM:135316034) increases p(HGNC:SOD1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:135316034) increases p(HGNC:SOD1) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") increases p(HGNC:SOD1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:SOD1) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:

p(HGNC:AMBP) decreases p(HGNC:SOD1) View Subject | View Object

Starvation led to a significantly down-regulation of the oxidative stress-related SOD1 (p,0.008) and catalase (p,0.043) in blood, but a 2.6-fold up-regulation of catalase in placenta (Figure 10A). PubMed:24489717

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Blood
Text Location
Results

Out-Edges 9

p(HGNC:SOD1) hasVariant p(HGNC:SOD1, var("p.Gly576Arg")) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

p(HGNC:SOD1) hasVariant p(HGNC:SOD1, pmod(HBP:misfolding)) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

p(HGNC:SOD1) decreases bp(GO:"response to oxidative stress") View Subject | View Object

The normal function of SOD1 is to scavenge oxygen radicals and prevent oxidative stress. PubMed:14556719

Appears in Networks:

p(HGNC:SOD1) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:

p(HGNC:SOD1) increases rxn(reactants(a(CHEBI:superoxide)), products(a(CHEBI:"hydrogen peroxide"), a(CHEBI:dioxygen))) View Subject | View Object

Primary cellular defensive mechanisms include enzymes like the superoxide dismutases, SOD1 (Cu–Zn SOD) and SOD2 (MnSOD) that convert superoxide to H 2 O 2 and catalase or glutathione peroxidase that convert H 2 O 2 to H 2 O; PubMed:24563850

Appears in Networks:

p(HGNC:SOD1) hasVariant p(HGNC:SOD1, var("p.Ala4Val")) View Subject | View Object

Appears in Networks:

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.