| Translational genetic approaches to substance use disorders: bridging the gap between mice and humans. | |
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MedLine Citation:
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PMID: 22170288 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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While substance abuse disorders only occur in humans, mice and other model organisms can make valuable contributions to genetic studies of these disorders. In this review, we consider a few specific examples of how model organisms have been used in conjunction with studies in humans to study the role of genetic factors in substance use disorders. In some examples genes that were first discovered in mice were subsequently studied in humans. In other examples genes or specific polymorphisms in genes were first studied in humans and then modeled in mice. Using anatomically and temporally specific genetic, pharmacological and other environmental manipulations in conjunction with histological analyses, mechanistic insights that would be difficult to obtain in humans have been obtained in mice. We hope these examples illustrate how novel biological insights about the effect of genes on substance use disorders can be obtained when mouse and human genetic studies are successfully integrated. |
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Authors:
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Abraham A Palmer; Harriet de Wit |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-12-15 |
Journal Detail:
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Title: Human genetics Volume: 131 ISSN: 1432-1203 ISO Abbreviation: Hum. Genet. Publication Date: 2012 Jun |
Date Detail:
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Created Date: 2012-05-15 Completed Date: 2012-07-20 Revised Date: 2013-04-01 |
Medline Journal Info:
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Nlm Unique ID: 7613873 Medline TA: Hum Genet Country: Germany |
Other Details:
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Languages: eng Pagination: 931-9 Citation Subset: IM |
Affiliation:
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Department of Human Genetics, The University of Chicago, Chicago, IL 60637, USA. aap@uchicago.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Carrier Proteins / genetics, metabolism Casein Kinase Iepsilon / genetics, metabolism Catechol O-Methyltransferase / genetics, metabolism Disease Models, Animal* Genetic Association Studies Genetic Variation* Humans Mice Phenotype* Receptor Protein-Tyrosine Kinases / genetics, metabolism Receptors, Nicotinic / genetics, metabolism Receptors, Opioid, mu / genetics, metabolism Species Specificity Substance-Related Disorders / genetics* |
| Grant Support | |
ID/Acronym/Agency:
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R01 DA021336/DA/NIDA NIH HHS; R01 DA021336-01/DA/NIDA NIH HHS; R01 DA021336-02/DA/NIDA NIH HHS; R01 DA021336-03/DA/NIDA NIH HHS; R01 DA021336-03S1/DA/NIDA NIH HHS; R01 DA021336-04/DA/NIDA NIH HHS; R01 DA021336-04S1/DA/NIDA NIH HHS; R01 DA021336-04S2/DA/NIDA NIH HHS; R01 DA021336-05/DA/NIDA NIH HHS; R01 DA021336-06/DA/NIDA NIH HHS; R01 DA021336-07/DA/NIDA NIH HHS; R01 GM097737-01A1/GM/NIGMS NIH HHS; R01 GM097737-02/GM/NIGMS NIH HHS; R01 MH079103-01/MH/NIMH NIH HHS; R01 MH079103-02/MH/NIMH NIH HHS; R01 MH079103-03/MH/NIMH NIH HHS; R01 MH079103-03S1/MH/NIMH NIH HHS; R01 MH079103-04/MH/NIMH NIH HHS; R01 MH079103-05/MH/NIMH NIH HHS; R01DA009133/DA/NIDA NIH HHS; R01DA021336/DA/NIDA NIH HHS; R01DA02812/DA/NIDA NIH HHS; R01DA032015/DA/NIDA NIH HHS; R01GM097737/GM/NIGMS NIH HHS; R01MH079103/MH/NIMH NIH HHS; R03 DA027545-01/DA/NIDA NIH HHS; R03 DA027545-02/DA/NIDA NIH HHS; R03DA027545/DA/NIDA NIH HHS; R21 DA024845-01/DA/NIDA NIH HHS; R21 DA024845-02/DA/NIDA NIH HHS; R21DA026570/DA/NIDA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Carrier Proteins; 0/Mpdz protein, mouse; 0/OPRM1 protein, human; 0/Receptors, Nicotinic; 0/Receptors, Opioid, mu; EC 2.1.1.6/Catechol O-Methyltransferase; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.10.1/anaplastic lymphoma kinase; EC 2.7.11.1/Casein Kinase Iepsilon |
| Comments/Corrections | |
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