Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

GENE - CHEMICAL INTERACTIONS REPORT

RGD ID: 735879
Species: Mus musculus
RGD Object: Gene
Symbol: Ache
Name: acetylcholinesterase
Acc ID: CHEBI:25710
Term: organophosphorus compound
Definition: An organophosphorus compound is formally a compound containing at least one carbon-phosphorus bond, but the term is often extended to include esters and thioesters.
Chemical ID: MESH:D009943
Note: Use of the qualifier "multiple interactions" designates that the annotated interaction is comprised of a complex set of reactions and/or regulatory events, possibly involving additional chemicals and/or gene products.
Object SymbolQualifierEvidenceWithReferenceSourceNotesOriginal Reference(s)
Achedecreases activityEXP 6480464CTDOrganophosphorus Compounds results in decreased activity of ACHE proteinPMID:27154493
Acheincreases metabolic processingEXP 6480464CTDACHE protein results in increased metabolism of Organophosphorus CompoundsPMID:22209767
Achedecreases activityISOACHE (Homo sapiens)6480464CTDOrganophosphorus Compounds analog results in decreased activity of ACHE protein; Organophosphorus Compounds results in decreased activity of ACHE proteinPMID:16807370 PMID:17098105 PMID:19793545 PMID:20096273 PMID:20105433 PMID:20303930 PMID:23557688 PMID:27154493
Achedecreases response to substanceISOACHE (Homo sapiens)6480464CTDACHE protein mutant form results in decreased susceptibility to Organophosphorus CompoundsPMID:20005217
Acheincreases metabolic processingISOACHE (Homo sapiens)6480464CTDACHE protein results in increased metabolism of Organophosphorus CompoundsPMID:22209767
Achemultiple interactionsISOACHE (Homo sapiens)6480464CTD[Organophosphorus Compounds results in decreased activity of ACHE protein] which results in increased abundance of Acetylcholine; asoxime chloride inhibits the reaction [Organophosphorus Compounds results in decreased activity of ACHE protein]; Atropine inhibits the reaction [[Organophosphorus Compounds results in decreased activity of ACHE protein] which results in increased abundance of Acetylcholine]; HLo 7 inhibits the reaction [Organophosphorus Compounds results in decreased activity of ACHE protein]; N,N'-monomethylenebis(pyridiniumaldoxime) inhibits the reaction [Organophosphorus Compounds results in decreased activity of ACHE protein]; Oximes inhibits the reaction [Organophosphorus Compounds results in decreased activity of ACHE protein]; pralidoxime inhibits the reaction [Organophosphorus Compounds results in decreased activity of ACHE protein]PMID:20096273 PMID:20105433 PMID:20156430
Go Back to source page   Continue to Ontology report