ArticleSchizophrenia bulletin2010
Supportive evidence for reduced expression of GNB1L in schizophrenia.
Article in Schizophrenia bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 31 citations in OpenAlex.
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- Analysis of genes within the schizophrenia-linked 22q11.2 deletion identifies interaction of night owl/LZTR1 and NF1 in GABAergic sleep control.PLoS genetics · 2020Article
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- The NSW brain tissue resource centre: Banking for alcohol and major neuropsychiatric disorders research.Alcohol (Fayetteville, N.Y.) · 2016Article
- The schizophrenia/bipolar disorder candidate gene GNB1L is regulated in human temporal cortex by a cis-acting element located within the 3'-region.Neuroscience bulletin · 2015Article
- Comparative mapping of the 22q11.2 deletion region and the potential of simple model organisms.Journal of neurodevelopmental disorders · 2015Article
- Copy number variation at 22q11.2: from rare variants to common mechanisms of developmental neuropsychiatric disorders.Molecular psychiatry · 2013Review
- DPP6 as a candidate gene for neuroleptic-induced tardive dyskinesia.The pharmacogenomics journal · 2013Article
- Convergent functional genomics of schizophrenia: from comprehensive understanding to genetic risk prediction.Molecular psychiatry · 2012Article
- Evidence for involvement of GNB1L in autism.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012Article
- Association of the HSPG2 gene with neuroleptic-induced tardive dyskinesia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010Article
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Authors and funding
23 authors at 11 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChromosome 22q11 deletion syndrome (22q11DS) increases the risk of development of schizophrenia more than 10 times compared with that of the general population, indicating that haploinsufficiency of a subset of the more than 20 genes contained in the 22q11DS region could increase the risk of schizophrenia. In the present study, we screened for genes located in the 22q11DS region that are expressed at lower levels in postmortem prefrontal cortex of patients with schizophrenia than in those of controls.
methodsGene expression was screened by Illumina Human-6 Expression BeadChip arrays and confirmed by real-time reverse transcription-polymerase chain reaction assays and Western blot analysis.
resultsExpression of GNB1L was lower in patients with schizophrenia than in control subjects in both Australian (10 schizophrenia cases and 10 controls) and Japanese (43 schizophrenia cases and 11 controls) brain samples. TBX1 could not be evaluated due to its low expression levels. Expression levels of the other genes were not significantly lower in patients with schizophrenia than in control subjects. Association analysis of tag single-nucleotide polymorphisms in the GNB1L gene region did not confirm excess homozygosity in 1918 Japanese schizophrenia cases and 1909 Japanese controls. Haloperidol treatment for 50 weeks increased Gnb1l gene expression in prefrontal cortex of mice.
conclusionsTaken together with the impaired prepulse inhibition observed in heterozygous Gnb1l knockout mice reported by the previous study, the present findings support assertions that GNB1L is one of the genes in the 22q11DS region responsible for increasing the risk of schizophrenia.
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