ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2011
SLC9A9 mutations, gene expression, and protein-protein interactions in rat models of attention-deficit/hyperactivity disorder.
Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Endosomal system genetics and autism spectrum disorders: A literature review.Neuroscience and biobehavioral reviews · 2016Pooled it
- Functional effects of dopamine transporter gene genotypes on in vivo dopamine transporter functioning: a meta-analysis.Molecular psychiatry · 2014Pooled it
- Correlation of AHR Activation-Induced Suppression of PWM-Stimulated IgG and IgG-Triggered Signaling in Human PBMCs.Antibodies (Basel, Switzerland) · 2026Article
- The Wistar-Kyoto rat as a model relevant to inattentive ADHD: substrain variability and affective comorbidity.Pharmacological reports : PR · 2026Review
- Cognitive Impairment and Synaptic Dysfunction in Cardiovascular Disorders: The New Frontiers of the Heart-Brain Axis.Biomedicines · 2024Review
- GGA1 interacts with the endosomal Na+/H+ exchanger NHE6 governing localization to the endosome compartment.The Journal of biological chemistry · 2024Article
- The known and unknown about attention deficit hyperactivity disorder (ADHD) genetics: a special emphasis on Arab population.Frontiers in genetics · 2024Review
- Attention-deficit/hyperactivity disorder and lifetime cannabis use: genetic overlap and causality.Molecular psychiatry · 2020Article
- Attention-Deficit/Hyperactivity Disorder Predominantly Inattentive Subtype/Presentation: Research Progress and Translational Studies.Brain sciences · 2020Review
- Genetics of attention deficit hyperactivity disorder.Molecular psychiatry · 2019Review
- Functional analysis of NaMatters · 2017Article
- NaThe Journal of biological chemistry · 2017Article
- 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
- Genetic architecture of Wistar-Kyoto rat and spontaneously hypertensive rat substrains from different sources.Physiological genomics · 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
- Emerging roles of Na⁺/H⁺ exchangers in epilepsy and developmental brain disorders.Progress in neurobiologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
SLC9A9 (solute carrier family 9, member 9, also known as Na+/H+ exchanger member (NHE9)) is a membrane protein that regulates the luminal pH of the recycling endosome, an essential organelle for synaptic transmission and plasticity. SLC9A9 has been implicated in human attention deficit hyperactivity disorder (ADHD) and in rat studies of hyperactivity. We examined the SLC9A9 gene sequence and expression profile in prefrontal cortex, dorsal striatum and hippocampus in two genetic rat models of ADHD. We report two mutations in a rat model of inattentive ADHD, the WKY/NCrl rat, which affect the interaction of SLC9A9 with calcineurin homologous protein (CHP). We observed an age-dependent abnormal expression of SLC9A9 in brains of this inattentive model and in the Spontaneous Hypertensive Rat (SHR) model of ADHD. Our data suggest a novel mechanism whereby SLC9A9 sequence variants and abnormalities in gene expression could contribute to the ADHD-like symptoms of rat models and possibly the pathophysiology of ADHD in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.