ArticlePsychiatric genetics2010
Genetic variants in SLC9A9 are associated with measures of attention-deficit/hyperactivity disorder symptoms in families.
Article in Psychiatric genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Functional effects of dopamine transporter gene genotypes on in vivo dopamine transporter functioning: a meta-analysis.Molecular psychiatry · 2014Pooled it
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- Assorted dysfunctions of endosomal alkali cation/proton exchangerThe Journal of biological chemistry · 2020Article
- Pathobiology of Christianson syndrome: Linking disrupted endosomal-lysosomal function with intellectual disability and sensory impairments.Neurobiology of learning and memory · 2019Article
- A recurrent missense variant in SLC9A7 causes nonsyndromic X-linked intellectual disability with alteration of Golgi acidification and aberrant glycosylation.Human molecular genetics · 2019Article
- The NaMolecular biology of the cell · 2018Article
- Genetic Variants and Multiple Sclerosis Risk Gene SLC9A9 Expression in Distinct Human Brain Regions.Molecular neurobiology · 2017Article
- Moving towards causality in attention-deficit hyperactivity disorder: overview of neural and genetic mechanisms.The lancet. Psychiatry · 2016Review
- Genetic and phenotypic diversity of NHE6 mutations in Christianson syndrome.Annals of neurology · 2014Article
- Endosomal pH in neuronal signaling and synaptic transmission: role of Na(+)/H(+) exchanger NHE5.Frontiers in physiology · 2014Review
- An inside job: how endosomal Na(+)/H(+) exchangers link to autism and neurological disease.Frontiers in cellular neuroscience · 2014Review
- Traditional and emerging roles for the SLC9 Na+/H+ exchangers.Pflugers Archiv : European journal of physiology · 2014Review
- A genome-wide association study of alcohol-dependence symptom counts in extended pedigrees identifies C15orf53.Molecular psychiatry · 2013Article
- Functional evaluation of autism-associated mutations in NHE9.Nature communications · 2013Article
- Small rare recurrent deletions and reciprocal duplications in 2q21.1, including brain-specific ARHGEF4 and GPR148.Human molecular genetics · 2012Article
- Differential expression of SLC9A9 and interacting molecules in the hippocampus of rat models for attention deficit/hyperactivity disorder.Developmental neuroscience · 2012Article
- SLC9A9 mutations, gene expression, and protein-protein interactions in rat models of attention-deficit/hyperactivity disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011Article
- X-linked Angelman-like syndrome caused by Slc9a6 knockout in mice exhibits evidence of endosomal-lysosomal dysfunction.Brain : a journal of neurology · 2011Article
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10 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveA family was previously identified that cosegregates a pericentric inversion, inv(3)(p14 : q21), with an early-onset developmental condition, characterized by impulsive behavior and intellectual deficit. The inversion breakpoints lie within DOCK3 and SLC9A9 at the p-arm and q-arm, respectively. Based on this report, these genes were selected to be evaluated in a family-based attention-deficit/hyperactivity disorder (AD/HD) association study.
methodsConners' Parent (CPRS) and Teacher (CTRS) Rating Scales of AD/HD symptoms and Conners' Continuous Performance Test (CPT) measures were collected and a minimal number of tagging single-nucleotide polymorphisms (SNPs) in each gene were selected for analysis. Analyses were performed on families who met research criteria for AD/HD. Using the program, QTDT, each tagging SNP was tested for association with T-scores from the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) subscales according to the CTRS and CPRS, and five CPT measures.
resultsAfter adjusting for multiple testing, a SNP in the 3' UTR of SLC9A9, rs1046706, remained significantly associated (false discovery rate, q value <0.05) with scores on the DSM-IV hyperactive-impulsive and total symptom subscales according to the CTRS and errors of commission on the CPT. In addition, an intronic SLC9A9 SNP, rs2360867, remained significantly associated with errors of commission.
conclusionOur results suggest that SLC9A9 may be related to hyperactive-impulsive symptoms in AD/HD and the disruption of SLC9A9 may be responsible for the behavioral phenotype observed in the inversion family. The association with SLC9A9 is particularly interesting as it was recently implicated in a genome-wide association study for AD/HD. Further investigation of the role of SLC9A9 in AD/HD and other behavioral disorders is warranted.
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