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p(HGNC:SOD2)

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Entity

Name
SOD2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 6

a(PUBCHEM:5757) increases p(HGNC:SOD2) View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

Appears in Networks:
Annotations
MeSH
Neurons

act(complex(GO:"NF-kappaB complex")) increases p(HGNC:SOD2) View Subject | View Object

NF-κB activation also protects hippocampal neurons from oxidative stress-induced apoptosis by inducing manganese superoxide dismutase (MnSOD) expression and mitigating peroxynitrite-induced protein nitration PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases p(HGNC:SOD2) View Subject | View Object

Furthermore, Amyloid-β –induced NF-κB also results in the up-regulation of the antioxidant mitochondrial membrane enzyme – MnSOD (superoxide dismutase 2) [328] which is well known to combat oxidative stress and apoptosis PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases act(p(HGNC:SOD2)) View Subject | View Object

In primary neuronal cells, exposure to Aβ25-35 peptide increase NF-κB mediated transactivation of manganese superoxide dismutase (Mn-SOD), suppress peroxinitrite production and inhibit membrane depolarization, thereby preventing apoptosis induced by oxidative stress PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:GRM5) increases act(p(HGNC:SOD2)) View Subject | View Object

In metabotrophic glutamate receptor-5 (mGlu5) agonist pretreated primary cortical neurons or neuroblastoma cells, Aβ induced toxicity was suppressed by selective activation of c-rel containing NF-κB dimers and transactivation of anti-apoptotic genes, Mn-SOD and Bcl-Xl [26] (Figs 1B, 2A) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:AMBP) increases p(HGNC:SOD2) View Subject | View Object

Treatment of starved ewes with A1M up-regulated the expression of SOD2 (p,0.043) and down-regulated the expression of s-Flt1 (p,0.012), in blood (Figure 11). PubMed:24489717

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

Out-Edges 4

p(HGNC:SOD2) 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:SOD2) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

Furthermore, Amyloid-β –induced NF-κB also results in the up-regulation of the antioxidant mitochondrial membrane enzyme – MnSOD (superoxide dismutase 2) [328] which is well known to combat oxidative stress and apoptosis PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:SOD2) decreases bp(GO:"apoptotic process") View Subject | View Object

Furthermore, Amyloid-β –induced NF-κB also results in the up-regulation of the antioxidant mitochondrial membrane enzyme – MnSOD (superoxide dismutase 2) [328] which is well known to combat oxidative stress and apoptosis PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(HGNC:SOD2)) decreases act(a(CHEBI:"amyloid-beta")) View Subject | View Object

In metabotrophic glutamate receptor-5 (mGlu5) agonist pretreated primary cortical neurons or neuroblastoma cells, Aβ induced toxicity was suppressed by selective activation of c-rel containing NF-κB dimers and transactivation of anti-apoptotic genes, Mn-SOD and Bcl-Xl [26] (Figs 1B, 2A) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

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.