ArticleNeurogenetics2005
The Gem interacting protein (GMIP) gene is associated with major depressive disorder.
Article in Neurogenetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Meta-analyses of genetic studies on major depressive disorder.Molecular psychiatry · 2008Pooled it
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- DNA modification study of major depressive disorder: beyond locus-by-locus comparisons.Biological psychiatry · 2015Article
- Poor replication of candidate genes for major depressive disorder using genome-wide association data.Molecular psychiatry · 2011Article
- Risk factors for the development of depression in patients with hepatitis C taking interferon-α.Neuropsychiatric disease and treatment · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Major depressive disorder (MDD) is a mood disorder with a significant heritable component. Structural neuronal impairment has been considered to be implicated in MDD, as it leads to brain morphological alterations such as hippocampal atrophy. The Gem interacting protein, GMIP, is a novel Rho GTPase-activating protein known to play important roles in neurite growth and axonal guidance. We examined the GMIP gene for possible association in a Japanese sample of 164 patients with MDD and 164 controls matched for sex. We found a significant association with MDD for one single nucleotide polymorphism (SNP) (-525G/A) located on the 5'-upstream region of the GMIP gene (p=0.039, odds ratio 1.66, 95% CI 1.05-2.69) and stronger evidence for association in a multimarker haplotype analysis (p=0.004). We then performed a promoter-luciferase reporter assay; the promoter activity for -525A allele, which was in excess in the MDD patients, was significantly decreased compared with the -525G allele in transient transfection experiments using three types of cell lines. Our results suggest that genetic variations in the GMIP gene can confer susceptibility to MDD, and the associated promoter SNP might play a role in the transcriptional regulation of the GMIP gene. Further study needs to be undertaken to validate the association between the GMIP gene and MDD.
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Registered trials
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