Common pathways underlying drug addiction (Homo sapiens)
From WikiPathways
Description
The pathway was modeled after Figure 2 in Li, et al. 2008 and is based on the common pathways identified in their study as well as protein interaction data. Specifically, glutamate and dopamine neuroactive ligand-receptor interactions trigger long-term potentiation, MAPK and GnRH signaling and gap junction regulation (green outlined pathway nodes). Related functional modules such as depolarization, gene expression and cytoskeleton regulation are also indicated (non-outlined pathway nodes). Among the several positive feedback loops identified in this pathway, the authors highlighted fast and slow ones in red and blue, respectively.
Proteins on this pathway have targeted assays available via the CPTAC Assay Portal
Quality Tags
Ontology Terms
Pathway Ontology : hyperprolinemia type II disease pathway disease pathway lysine degradation pathway hypophosphatasia disease pathway vitamin B6 metabolic pathway proline metabolic pathway
Disease : hypophosphatasia epilepsy infantile hypophosphatasia hyperprolinemia type 2 early-onset vitamin B6-dependent epilepsy childhood hypophosphatasia pyridoxamine 5'-phosphate oxidase deficiency pyridoxine-dependent epilepsy
Cell Type : neural cell
Bibliography
- Li CY, Mao X, Wei L; ''Genes and (common) pathways underlying drug addiction.''; PLoS Comput Biol, 2008 PubMed Europe PMC Scholia
History
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External references
DataNodes
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Annotated Interactions
No annotated interactions