ArticleProgress in neuro-psychopharmacology & biological psychiatry2010
Association analysis between polymorphisms in the myo-inositol monophosphatase 2 (IMPA2) gene and bipolar disorder.
Article in Progress in neuro-psychopharmacology & biological psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Mechanisms of Lithium Action: The Old and New Findings.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Myo-inositol rescued insulin resistance and dyslipidemia in db/db mice.Journal of applied biomedicine · 2024Article
- Comparative transcriptome and methylome of polar bears, giant and red pandas reveal diet-driven adaptive evolution.Evolutionary applications · 2024Article
- IMPA2 blocks cervical cancer cell apoptosis and induces paclitaxel resistance through p53-mediated AIFM2 regulation.Acta biochimica et biophysica Sinica · 2023Article
- Inositol monophosphatase 2 promotes epithelial ovarian cancer cell proliferation and migration by regulating the AKT/mTOR signaling pathway.Experimental and therapeutic medicine · 2022Article
- Identification of IMPA2 as the hub gene associated with colorectal cancer and liver metastasis by integrated bioinformatics analysis.Translational oncology · 2022Article
- Dysregulation of the miR-25-IMPA2 axis promotes metastatic progression in clear cell renal cell carcinoma.EBioMedicine · 2019Article
- Molecular actions and clinical pharmacogenetics of lithium therapy.Pharmacology, biochemistry, and behavior · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Linkage studies in bipolar disorder (BPD) suggest that a susceptibility locus exists on chromosome 18p11. The myo-inositol monophosphatase 2 gene (IMPA2) maps to this genomic region. Myo-inositol monophosphatase dephosphorylates inositol monophosphate, regenerating free inositol. Lithium, a common treatment for BPD, has been shown to inhibit IMPA2 activity and decrease levels of inositol. It is hypothesized that lithium conveys its therapeutic effect for BPD patients partially through inositol regulation. Hence, dysfunction of inositol caused by IMPA2 irregularity may contribute to the pathophysiology of BPD. In this study, we hypothesize that genetic variations in the IMPA2 gene contributes to increased susceptibility to BPD. We tested this hypothesis by genotyping 9 SNPs (rs1787984; rs585247; rs3974759; rs650727; rs589247; rs669838; rs636173; rs3786285; rs613993) in BPD patients (n=556) and controls (n=735). Genotype and allele frequencies were compared between groups using Chi square contingency analysis. Linkage disequilibrium (LD) between markers was calculated and estimated haplotype frequencies were compared between groups. Single marker analysis revealed several associations between IMPA2 variations and BPD, which were subsequently rendered non-significant after correction for multiple testing. Although our study did not show strong support for an association between the tested IMPA2 polymorphisms and susceptibility to BPD, additional larger studies are necessary to comprehensively investigate a role of the IMPA2 gene in the pathophysiology of BPD.
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