Portal:AOP/Mission
From WikiPathways
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The proposed list of the first set of AOPs to be created, some are more defined than others: | The proposed list of the first set of AOPs to be created, some are more defined than others: | ||
| - | * | + | * Chemical-induced bile duct obstruction leads to liver failure |
| - | * | + | * Chemical-induced bile duct obstruction leads to nephrotoxicity |
| - | * | + | * Inhibition of N-linked glycosylation leads to liver injury |
| - | * | + | * Mitochondrial complex inhibition leading to liver injury |
* Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits | * Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits | ||
* Peripheral neuropathy caused by microtubule interacting drugs | * Peripheral neuropathy caused by microtubule interacting drugs | ||
* Oxidative reactivity leads to chemical-induced fanconi syndrome | * Oxidative reactivity leads to chemical-induced fanconi syndrome | ||
| - | * | + | * Binding to complex I of the electron transport chain leading to chemical-induced Fanconi syndrome |
| - | * | + | * Intracellular accumulation of chemicals via the megalin/cubulin system leading to tubulonephritis |
| - | + | ||
* Oxidant-induced pulmonary emphysema | * Oxidant-induced pulmonary emphysema | ||
* α-diketone-induced bronchiolitis obliterans | * α-diketone-induced bronchiolitis obliterans | ||
* HDAC inhibition leads to neural tube defects | * HDAC inhibition leads to neural tube defects | ||
| - | * | + | * Cyp17 inhibition leads to undescended testes |
| - | + | * Oxidative stress-induced liver injury | |
| - | * Oxidative stress-induced | + | * IKK complex inhibition leads to liver failure |
| - | * | + | |
* HDAC inhibition leads to impaired craniofacial development | * HDAC inhibition leads to impaired craniofacial development | ||
Revision as of 11:06, 19 December 2017
The purpose of this portal is to create a collection of AOPs on the molecular level for the AOPs that are, or will be created for the EU-ToxRisk program, in which Open PHACTS Foundation (OPF) is responsible for AOP creation. The subjects of the first AOPs are linked to the use cases of the EU-ToxRisk program, and there will be a team of experts involved in the creation of each AOP.
The proposed list of the first set of AOPs to be created, some are more defined than others:
- Chemical-induced bile duct obstruction leads to liver failure
- Chemical-induced bile duct obstruction leads to nephrotoxicity
- Inhibition of N-linked glycosylation leads to liver injury
- Mitochondrial complex inhibition leading to liver injury
- Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits
- Peripheral neuropathy caused by microtubule interacting drugs
- Oxidative reactivity leads to chemical-induced fanconi syndrome
- Binding to complex I of the electron transport chain leading to chemical-induced Fanconi syndrome
- Intracellular accumulation of chemicals via the megalin/cubulin system leading to tubulonephritis
- Oxidant-induced pulmonary emphysema
- α-diketone-induced bronchiolitis obliterans
- HDAC inhibition leads to neural tube defects
- Cyp17 inhibition leads to undescended testes
- Oxidative stress-induced liver injury
- IKK complex inhibition leads to liver failure
- HDAC inhibition leads to impaired craniofacial development
Basic strategies and principles for general AOPs are described in this paper:
Villeneuve et al. (2014). Adverse Outcome Pathway (AOP) Development I: Strategies and Principles. Toxicological Sciences PubMed
