CIDeRGeneral Information:
| Id: | 404 (click here to show other Interactions for entry) |
| Diseases: |
Amyotrophic lateral sclerosis
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| Mus musculus | |
| SOD1G93A transgenic mouse, transfected with human SOD1G93A | |
| BTO:0000078 microglia | |
| article | |
| Reference: | D'Ambrosi N et al.(2009) The proinflammatory action of microglial P2 receptors is enhanced in SOD1 models for amyotrophic lateral sclerosis J. Immunol. 183: 4648-4656 [PMID: 19734218] |
Interaction Information:
| Comment | Under basal conditions, the expression of TNF-alpha was increased in immortalized hSOD1-G93A microglia, with respect to nontransgenic cells. The addition of extracellular ATP and BzATP (2'-3'-O-(benzoyl-benzoyl) ATP) increased TNF-alpha content in all cases, but with a higher level of induction in immortalized and primary hSOD1-G93A cells. |
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Formal Description Interaction-ID: 1732 |
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| Drugbank entries | Show/Hide entries for TNF |
| Comment | The addition of extracellular ATP and BzATP (the most effective agonist) increased TNF-alpha content in all cases, but with a higher level of induction in immortalized and primary hSOD1-G93A cells. In general, BzATP was always more potent than ATP in increasing overall TNF-alpha content, with maximum levels reached in ALS-linked immortalized and primary cells. |
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Formal Description Interaction-ID: 13527 |
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| Drugbank entries | Show/Hide entries for TNF |
| Comment | The addition of extracellular ATP and BzATP (the most effective agonist) increased TNF-alpha content in all cases, but with a higher level of induction in immortalized and primary hSOD1-G93A cells. In general, BzATP was always more potent than ATP in increasing overall TNF-alpha content, with maximum levels reached in ALS-linked immortalized and primary cells. |
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Formal Description Interaction-ID: 13546 |
drug/chemical compound increases_quantity of gene/protein |
| Drugbank entries | Show/Hide entries for TNF |