Portal:AOP/Mission
From WikiPathways
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
The list of Featured Pathways is not static and can be updated at any time. If you know of a pathway that should be added, please contact Marvin Martens.