ArticleBiological psychiatry2016
An Ultraconserved Brain-Specific Enhancer Within ADGRL3 (LPHN3) Underpins Attention-Deficit/Hyperactivity Disorder Susceptibility.
Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Meta-analysis and systematic review of ADGRL3 (LPHN3) polymorphisms in ADHD susceptibility.Molecular psychiatry · 2021Pooled it
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Genetic structure and selective signatures revealed by whole genome sequencing in potato grouper (Epinephelus tukula).BMC genomics · 2026Article
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- A method for structure determination of GPCRs in various states.Nature chemical biology · 2024Article
- Impulsive choice in two different rat models of ADHD-Spontaneously hypertensive andFrontiers in neuroscience · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- ADGRL3 genomic variation implicated in neurogenesis and ADHD links functional effects to the incretin polypeptide GIP.Scientific reports · 2022Article
- Latrophilin-3 heterozygous versus homozygous mutations in Sprague Dawley rats: Effects on egocentric and allocentric memory and locomotor activity.Genes, brain, and behavior · 2022Article
- ADGRL1 haploinsufficiency causes a variable spectrum of neurodevelopmental disorders in humans and alters synaptic activity and behavior in a mouse model.American journal of human genetics · 2022Article
- Driver mutations in ADGRL3 are involved in the evolution of ependymoma.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Convergent selective signaling impairment exposes the pathogenicity of latrophilin-3 missense variants linked to inheritable ADHD susceptibility.Molecular psychiatry · 2022Article
- Case Report of a Juvenile Patient with Autism Spectrum Disorder with a Novel Combination of Copy Number Variants inThe application of clinical genetics · 2022Article
- An assessment of executive function in two different rat models of attention-deficit hyperactivity disorder: Spontaneously hypertensive versus Lphn3 knockout rats.Genes, brain, and behavior · 2021Article
- Latrophilin-3 disruption: Effects on brain and behavior.Neuroscience and biobehavioral reviews · 2021Review
- Article
- Adhesion G protein-coupled receptor L3 gene variants: Statistically significant association observed in the male Indo-caucasoid Attention deficit hyperactivity disorder probands.Molecular biology reports · 2021Article
- Chromosomal Microarray Analysis as First-Tier Genetic Test for Schizophrenia.Frontiers in genetics · 2021Article
- Selection signatures of Fuzhong Buffalo based on whole-genome sequences.BMC genomics · 2020Article
- Mutations in sphingolipid metabolism genes are associated with ADHD.Translational psychiatry · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundGenetic factors predispose individuals to attention-deficit/hyperactivity disorder (ADHD). Previous studies have reported linkage and association to ADHD of gene variants within ADGRL3. In this study, we functionally analyzed noncoding variants in this gene as likely pathological contributors.
methodsIn silico, in vitro, and in vivo approaches were used to identify and characterize evolutionary conserved elements within the ADGRL3 linkage region (~207 Kb). Family-based genetic analyses of 838 individuals (372 affected and 466 unaffected patients) identified ADHD-associated single nucleotide polymorphisms harbored in some of these conserved elements. Luciferase assays and zebrafish green fluorescent protein transgenesis tested conserved elements for transcriptional enhancer activity. Electromobility shift assays were used to verify transcription factor-binding disruption by ADHD risk alleles.
resultsAn ultraconserved element was discovered (evolutionary conserved region 47) that functions as a transcriptional enhancer. A three-variant ADHD risk haplotype in evolutionary conserved region 47, formed by rs17226398, rs56038622, and rs2271338, reduced enhancer activity by 40% in neuroblastoma and astrocytoma cells (p
conclusionsThese results uncover the first functional evidence of common noncoding variants with potential implications for the pathology of ADHD.
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