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Appears in Networks 5

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

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

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

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

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

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

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erythrocyte
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Blood
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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

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

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

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

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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.