Difference between revisions of "Aop:58"
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__NOTOC__ | __NOTOC__ | ||
− | + | = Status = | |
− | {{ | + | <span style="color:#FF0000"> |
+ | This is a legacy representation of this AOP. Please see the current version here: | ||
+ | |||
+ | [//{{SERVERNAME}}/aops/58 https://{{SERVERNAME}}/aops/58] | ||
+ | </span> | ||
+ | |||
+ | |||
== AOP Title == | == AOP Title == | ||
− | <div id='longTitle' class='Title'> | + | <div id='longTitle' class='Title'> NR1I3 (CAR) suppression leading to hepatic steatosis </div> |
− | <div id='shortTitle' class='Title2'> Short name: | + | <div id='shortTitle' class='Title2'> Short name: NR1I3 suppression to steatosis </div> |
== Authors == | == Authors == | ||
+ | Michelle Angrish, Brian Chorley | ||
== Status == | == Status == | ||
+ | |||
+ | '''Please follow the link to [//{{SERVERNAME}}/aops/{{PAGENAMEE}}/snapshots snapshots page] to view and create Snapshots of this AOP.''' | ||
+ | |||
+ | [http://www.oecd.org/env/ehs/testing/listsofprojectsontheaopdevelopmentprogrammeworkplan.htm OECD Project 1.29: A catalog of putative AOPs that will enhance the utility of US EPA Toxcast high throughput screening data for hazard identification] | ||
+ | |||
'''Under development: Do not distribute or cite.''' | '''Under development: Do not distribute or cite.''' | ||
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== Summary of the AOP == | == Summary of the AOP == | ||
[[Category:Adverse Outcome Pathway]] | [[Category:Adverse Outcome Pathway]] | ||
− | Please follow link to [//{{SERVERNAME}} | + | Please follow link to [//{{SERVERNAME}}/aops/{{PAGENAMEE}} widget page] to edit this section. |
+ | |||
+ | <span style="color:#FF0000">'''If you manually enter text in this section, it will get automatically altered or deleted in subsequent edits using the widgets.'''</span> | ||
=== Molecular Initiating Event === | === Molecular Initiating Event === | ||
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|[[Event:456|Constitutive androstane receptor, NR1l3, Suppression]]||[[Aop:58#Essentiality of the Key Events|Moderate]] | |[[Event:456|Constitutive androstane receptor, NR1l3, Suppression]]||[[Aop:58#Essentiality of the Key Events|Moderate]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:468|PPAR alpha, Inhibition]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:167|LXR, Activation]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:228|PPARγ, Activation]]|| | ||
|- | |- | ||
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|- | |- | ||
− | |[[Event: | + | |[[Event:457|SREBF1, Activation]]||[[Aop:58#Essentiality of the Key Events|Moderate]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:66|ChREBP, Activation]]||[[Aop:58#Essentiality of the Key Events|Moderate]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:458|De Novo FA synthesis, Increased]]||[[Aop:58#Essentiality of the Key Events|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:460|Fatty acid uptake, Increased]]||[[Aop:58#Essentiality of the Key Events|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:454|Triglyceride formation, Increased]]||[[Aop:58#Essentiality of the Key Events|Moderate]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:54|CD36, Up Regulation]]||[[Aop:58#Essentiality of the Key Events|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:462|SCD-1, Up Regulation]]||[[Aop:58#Essentiality of the Key Events|Strong]] |
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:463|FAS, Up Regulation]]||[[Aop:58#Essentiality of the Key Events|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:451|Mitochondrial fatty acid beta-oxidation, Inhibition]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:327|Fatty acid, Accumulation]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:470|Acetyl-CoA carboxylase-1 (ACC-1), Up Regulation]]||[[Aop:58#Essentiality of the Key Events|Strong]] | ||
|- | |- | ||
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|- | |- | ||
− | |[[Event:456|Constitutive androstane receptor, NR1l3, Suppression]]||[[Relationship:477|Directly Leads to]]||[[Event:228| | + | |[[Event:456|Constitutive androstane receptor, NR1l3, Suppression]]||[[Relationship:477|Directly Leads to]]||[[Event:228|PPARγ, Activation]]||[[Relationship:477#Weight of Evidence|Strong]]||[[Relationship:477#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event:167|LXR, Activation]]||[[Relationship: | + | |[[Event:167|LXR, Activation]]||[[Relationship:479|Directly Leads to]]||[[Event:457|SREBF1, Activation]]||[[Relationship:479#Weight of Evidence|Strong]]||[[Relationship:479#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event:167|LXR, Activation]]||[[Relationship: | + | |[[Event:167|LXR, Activation]]||[[Relationship:174|Directly Leads to]]||[[Event:66|ChREBP, Activation]]||[[Relationship:174#Weight of Evidence|Strong]]||[[Relationship:174#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:66|ChREBP, Activation]]||[[Relationship:483|Directly Leads to]]||[[Event:458|De Novo FA synthesis, Increased]]||[[Relationship:483#Weight of Evidence|Strong]]||[[Relationship:483#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:454|Triglyceride formation, Increased]]||[[Relationship:486|Directly Leads to]]||[[Event:459|Liver Steatosis, Increased]]||[[Relationship:486#Weight of Evidence|Strong]]||[[Relationship:486#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:228|PPARγ, Activation]]||[[Relationship:487|Directly Leads to]]||[[Event:457|SREBF1, Activation]]||[[Relationship:487#Weight of Evidence|Moderate]]||[[Relationship:487#Quantitative Understanding of the Linkage|Moderate]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:228|PPARγ, Activation]]||[[Relationship:488|Directly Leads to]]||[[Event:460|Fatty acid uptake, Increased]]||[[Relationship:488#Weight of Evidence|Moderate]]||[[Relationship:488#Quantitative Understanding of the Linkage|Moderate]] |
|- | |- | ||
− | |[[Event: | + | |[[Event:457|SREBF1, Activation]]||[[Relationship:489|Directly Leads to]]||[[Event:462|SCD-1, Up Regulation]]||[[Relationship:489#Weight of Evidence|Strong]]||[[Relationship:489#Quantitative Understanding of the Linkage|Strong]] |
|- | |- | ||
− | |[[Event:454|Triglyceride formation, Increased]]||[[Relationship: | + | |[[Event:167|LXR, Activation]]||[[Relationship:173|Directly Leads to]]||[[Event:54|CD36, Up Regulation]]||[[Relationship:173#Weight of Evidence|Strong]]||[[Relationship:173#Quantitative Understanding of the Linkage|Strong]] |
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:167|LXR, Activation]]||[[Relationship:490|Directly Leads to]]||[[Event:463|FAS, Up Regulation]]||[[Relationship:490#Weight of Evidence|Strong]]||[[Relationship:490#Quantitative Understanding of the Linkage|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:167|LXR, Activation]]||[[Relationship:491|Directly Leads to]]||[[Event:462|SCD-1, Up Regulation]]||[[Relationship:491#Weight of Evidence|Strong]]||[[Relationship:491#Quantitative Understanding of the Linkage|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:463|FAS, Up Regulation]]||[[Relationship:492|Directly Leads to]]||[[Event:458|De Novo FA synthesis, Increased]]||[[Relationship:492#Weight of Evidence|Strong]]||[[Relationship:492#Quantitative Understanding of the Linkage|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:462|SCD-1, Up Regulation]]||[[Relationship:493|Directly Leads to]]||[[Event:454|Triglyceride formation, Increased]]||[[Relationship:493#Weight of Evidence|Strong]]||[[Relationship:493#Quantitative Understanding of the Linkage|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:54|CD36, Up Regulation]]||[[Relationship:494|Directly Leads to]]||[[Event:460|Fatty acid uptake, Increased]]||[[Relationship:494#Weight of Evidence|Strong]]||[[Relationship:494#Quantitative Understanding of the Linkage|Strong]] | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:167|LXR, Activation]]||[[Relationship:510|Indirectly Leads to]]||[[Event:468|PPAR alpha, Inhibition]]|||| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:468|PPAR alpha, Inhibition]]||[[Relationship:511|Directly Leads to]]||[[Event:451|Mitochondrial fatty acid beta-oxidation, Inhibition]]||[[Relationship:511#Weight of Evidence|Strong]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:458|De Novo FA synthesis, Increased]]||[[Relationship:512|Directly Leads to]]||[[Event:327|Fatty acid, Accumulation]]||[[Relationship:512#Weight of Evidence|Strong]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:460|Fatty acid uptake, Increased]]||[[Relationship:513|Directly Leads to]]||[[Event:327|Fatty acid, Accumulation]]||[[Relationship:513#Weight of Evidence|Strong]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:327|Fatty acid, Accumulation]]||[[Relationship:514|Directly Leads to]]||[[Event:454|Triglyceride formation, Increased]]|||| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:327|Fatty acid, Accumulation]]||[[Relationship:515|Directly Leads to]]||[[Event:459|Liver Steatosis, Increased]]|||| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:451|Mitochondrial fatty acid beta-oxidation, Inhibition]]||[[Relationship:475|Directly Leads to]]||[[Event:327|Fatty acid, Accumulation]]|||| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:167|LXR, Activation]]||[[Relationship:516|Directly Leads to]]||[[Event:470|Acetyl-CoA carboxylase-1 (ACC-1), Up Regulation]]||[[Relationship:516#Weight of Evidence|Strong]]|| | ||
+ | |||
+ | |- | ||
+ | |||
+ | |[[Event:470|Acetyl-CoA carboxylase-1 (ACC-1), Up Regulation]]||[[Relationship:517|Indirectly Leads to]]||[[Event:458|De Novo FA synthesis, Increased]]||[[Relationship:517#Weight of Evidence|Strong]]|| | ||
|- | |- | ||
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!Evidence | !Evidence | ||
!Links | !Links | ||
+ | |||
+ | |- | ||
+ | |||
+ | |human, mouse, rat||||[[Aop:58#Domain of Applicability|Moderate]]|| | ||
|- | |- |
Latest revision as of 19:06, 11 December 2016
Status
This is a legacy representation of this AOP. Please see the current version here:
AOP Title
Authors
Michelle Angrish, Brian Chorley
Status
Please follow the link to snapshots page to view and create Snapshots of this AOP.
Under development: Do not distribute or cite.
This AOP page was last modified on 12/11/2016.
Click here to show/hide revision dates for related pages
Page | Revision Date/Time |
---|
Abstract
Background (optional)
Summary of the AOP
Please follow link to widget page to edit this section.
If you manually enter text in this section, it will get automatically altered or deleted in subsequent edits using the widgets.
Molecular Initiating Event
Molecular Initiating Event | Support for Essentiality |
---|---|
Constitutive androstane receptor, NR1l3, Suppression | Moderate |
PPAR alpha, Inhibition | |
LXR, Activation | |
PPARγ, Activation |
Key Events
Adverse Outcome
Adverse Outcome |
---|
Liver Steatosis, Increased |
Relationships Among Key Events and the Adverse Outcome
Network View
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Life Stage Applicability
Life Stage | Evidence | Links |
---|
Taxonomic Applicability
Name | Scientific Name | Evidence | Links |
---|---|---|---|
human, mouse, rat | Moderate |
Sex Applicability
Sex | Evidence | Links |
---|
Graphical Representation
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Overall Assessment of the AOP
Domain of Applicability
Life Stage Applicability,
Taxonomic Applicability,
Sex Applicability
Elaborate on the domains of applicability listed in the summary section above. Specifically, provide the literature supporting, or excluding, certain domains.
Essentiality of the Key Events
Molecular Initiating Event Summary,
Key Event Summary
Provide an overall assessment of the essentiality for the key events in the AOP. Support calls for individual key events can be included in the molecular initiating event, key event, and adverse outcome tables above.
Weight of Evidence Summary
Summary Table
Provide an overall summary of the weight of evidence based on the evaluations of the individual linkages from the Key Event Relationship pages.
Quantitative Considerations
Summary Table
Provide an overall discussion of the quantitative information available for this AOP. Support calls for the individual relationships can be included in the Key Event Relationship table above.