Portal:AOP/Mission

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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.
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The purpose of this portal is to create a collection of AOPs on the molecular level and facilitating the use of high-throughput transcriptomic data in the AOP framework. The subjects of the first AOPs are linked to the use cases of the EU-ToxRisk program, based on [aopwiki.org AOP-Wiki] entries, and the CIAO project on COVID-19 AOPs.  
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List of molecular AOPs present in this portal (some are more defined than others):
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The proposed list of the first set of AOPs to be created, some are more defined than others:
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* Mitochondrial Complex I inhibition leads to liver injury
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* Mitochondrial Complex I inhibition leads to parkinsonian motor deficits
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* Chemical-induced bile duct obstruction leads to liver failure
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* Mitochondrial Complex I inhibition leads to Fanconi syndrome
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* Chemical-induced bile duct obstruction leads to nephrotoxicity
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* Protein alkylation leads to liver fibrosis
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* Inhibition of N-linked glycosylation leads to liver injury
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* Interaction with lung resident cell membrane components leads to lung fibrosis
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* Mitochondrial complex inhibition leading to liver injury
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* Multiple MIEs lead to liver steatosis
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* Inhibition of mitochondrial complex I of nigra-striatal neurons leads to parkinsonian motor deficits
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* ACE2 inhibition leads to increased mortality
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* Peripheral neuropathy caused by microtubule interacting drugs
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* Oxidative reactivity leads to chemical-induced fanconi syndrome
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* Binding to complex I of the electron transport chain leading to chemical-induced Fanconi syndrome
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* Intracellular accumulation of chemicals via the megalin/cubulin system leading to tubulonephritis
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* Oxidant-induced pulmonary emphysema
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* α-diketone-induced bronchiolitis obliterans
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* HDAC inhibition leads to neural tube defects
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* Cyp17 inhibition leads to undescended testes
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* Oxidative stress-induced liver injury
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* IKK complex inhibition leads to liver failure
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* HDAC inhibition leads to impaired craniofacial development
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Revision as of 12:03, 6 January 2021

The purpose of this portal is to create a collection of AOPs on the molecular level and facilitating the use of high-throughput transcriptomic data in the AOP framework. The subjects of the first AOPs are linked to the use cases of the EU-ToxRisk program, based on [aopwiki.org AOP-Wiki] entries, and the CIAO project on COVID-19 AOPs.

List of molecular AOPs present in this portal (some are more defined than others):

  • Mitochondrial Complex I inhibition leads to liver injury
  • Mitochondrial Complex I inhibition leads to parkinsonian motor deficits
  • Mitochondrial Complex I inhibition leads to Fanconi syndrome
  • Protein alkylation leads to liver fibrosis
  • Interaction with lung resident cell membrane components leads to lung fibrosis
  • Multiple MIEs lead to liver steatosis
  • ACE2 inhibition leads to increased mortality


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.

Retrieved from "https://classic.wikipathways.org/index.php/Portal:AOP/Mission"
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