ArticleMolecular psychiatry2010
Proteomic-based genotyping in a mouse model of trait anxiety exposes disease-relevant pathways.
Article in Molecular psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 39 citations in OpenAlex.
- Collective interaction effects associated with mammalian behavioral traits reveal genetic factors connecting fear and hemostasis.BMC psychiatry · 2018Article
- Downregulation of Spermine Augments Dendritic Persistent Sodium Currents and Synaptic Integration after Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Biomarkers for Psychiatry: The Journey from Fantasy to Fact, a Report of the 2013 CINP Think Tank.The international journal of neuropsychopharmacology · 2015Review
- Effect of an anti-depressant on mouse hippocampus protein turnover using MIMS.Surface and interface analysis : SIA · 2014Article
- Anxiety genetics - findings from cross-species genome-wide approaches.Biology of mood & anxiety disorders · 2013Article
- The diagnosis of depression: current and emerging methods.Comprehensive psychiatry · 2013Article
- The endocrine stress response is linked to one specific locus on chromosome 3 in a mouse model based on extremes in trait anxiety.BMC genomics · 2012Article
- Role of Glyoxalase 1 (Glo1) and methylglyoxal (MG) in behavior: recent advances and mechanistic insights.Frontiers in genetics · 2012Article
- Proteomics as a tool for understanding schizophrenia.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2011Article
- Profiling trait anxiety: transcriptome analysis reveals cathepsin B (Ctsb) as a novel candidate gene for emotionality in mice.PloS one · 2011Article
- The role of proteomics in depression research.European archives of psychiatry and clinical neuroscience · 2010Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our biomarker identification efforts, we have reported earlier on a protein that differs in its electrophoretic mobility between mouse lines bred either for high or low trait anxiety. The altered electrophoretic behavior of enolase phosphatase (EP) is now identified to be caused by two single-nucleotide polymorphisms. In both cases, the genetic polymorphism introduces an amino acid change in the protein's sequence resulting in differential mobility on SDS gels. This was shown by recombinantly expressing the two EP isoforms. Functional studies indicate that the EP isoform from the high anxiety mouse line has a lower enzymatic activity than does its low anxiety mouse counterpart. EP is a member of the methionine salvage pathway that is responsible for the synthesis of S-adenosyl-L-methionine, a natural compound with potential antidepressant activities. In addition, it is linked to the polyamine pathway whose members have functions in anxiety/depression-related behaviors. In a freely-segregating F2 panel, both single-nucleotide polymorphisms were significantly associated with locomotion-independent trait anxiety, further supporting a functional role of EP for this phenotype. The study shows that proteomic analysis can reveal genotypic differences relevant for the phenotype. The identified protein alterations, in turn, can expose metabolic pathways pertinent to the behavioral phenotype.
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