User:Marvin M2/AOPportal/Mission
From WikiPathways
< User:Marvin M2 | AOPportal(Difference between revisions)
(New page: 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 [http://www.eu-toxrisk.eu/ EU-ToxR...) |
Current revision (10:24, 31 March 2017) (view source) |
||
| (13 intermediate revisions not shown.) | |||
| Line 1: | Line 1: | ||
| - | The purpose | + | 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 [http://www.eu-toxrisk.eu/ EU-ToxRisk] program, in which [http://www.openphactsfoundation.org/ 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 | + | |
| - | * | + | |
| - | * | + | The proposed list of the first set of AOPs to be created: |
| - | * | + | |
| - | * | + | * 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'' [https://www.ncbi.nlm.nih.gov/pubmed/25466378 PubMed] | ||
Current revision
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:
- 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
