User:Marvin M2/AOPportal/Mission
From WikiPathways
(Difference between revisions)
| Line 3: | Line 3: | ||
The proposed list of the first set of AOPs is: | The proposed list of the first set of AOPs is: | ||
| - | * | + | * Inhibition of β-oxidation leads to liver steatosis |
| - | * | + | * HDAC inhibition, folate antagonism, oxidative stress and foetus accumulation lead to teratogenicity |
| - | * | + | * Oxidative stress leads to hepatotoxicity |
| - | * | + | * Oxidative stress leads to nephrotoxicity |
| - | * | + | * Disturbance of the respiratory chain leads to mitotoxicity |
| - | * | + | * PPAR activation leads to hepatoxicity |
| - | * | + | * OAT overactivation leads to nephrotoxicity |
| - | * | + | * PXR activation leads to liver steatosis |
| - | + | * NAPQI production causes hepatotoxicity | |
| + | * MTP impairment leads to hepatotoxicity | ||
| + | * CYP51 inhibition causes embryotoxicity | ||
| + | * Epithelial damage leads to popcorn lung | ||
Basic strategies and principles for general AOPs are described in this paper: | 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'' [https://www.ncbi.nlm.nih.gov/pubmed/25466378 PubMed] | Villeneuve ''et al.'' (2014). Adverse Outcome Pathway (AOP) Development I: Strategies and Principles. ''Toxicological Sciences'' [https://www.ncbi.nlm.nih.gov/pubmed/25466378 PubMed] | ||
Revision as of 14:27, 30 March 2017
The purpose behind the creation 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 subject of the first set of 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 is:
- Inhibition of β-oxidation leads to liver steatosis
- HDAC inhibition, folate antagonism, oxidative stress and foetus accumulation lead to teratogenicity
- Oxidative stress leads to hepatotoxicity
- Oxidative stress leads to nephrotoxicity
- Disturbance of the respiratory chain leads to mitotoxicity
- PPAR activation leads to hepatoxicity
- OAT overactivation leads to nephrotoxicity
- PXR activation leads to liver steatosis
- NAPQI production causes hepatotoxicity
- MTP impairment leads to hepatotoxicity
- CYP51 inhibition causes embryotoxicity
- Epithelial damage leads to popcorn lung
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
