ArticlePLoS genetics2014
Mutation of SLC35D3 causes metabolic syndrome by impairing dopamine signaling in striatal D1 neurons.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Integrated transcriptomic and proteomic validation identifies SLC35D3 as a tumor-selective surface antigen for colorectal and neuroendocrine carcinomas.Biochemistry and biophysics reports · 2026Article
- Secondary analysis of GenRED data (Genetics of Recurrent Early-Onset major Depression) using MERLIN.European archives of psychiatry and clinical neuroscience · 2026Article
- Transcriptomic profile of the hippocampus of rat strains with contrasting nervous system excitability.PloS one · 2026Article
- SLC35D3 promotes white adipose tissue browning to ameliorate obesity by NOTCH signaling.Nature communications · 2023Article
- Trace Amine-Associated Receptors and Monoamine-Mediated Regulation of Insulin Secretion in Pancreatic Islets.Biomolecules · 2023Review
- DNA methylation and hydroxymethylation characterize the identity of D1 and D2 striatal projection neurons.Communications biology · 2022Article
- Localization, proteomics, and metabolite profiling reveal a putative vesicular transporter for UDP-glucose.eLife · 2021Article
- HPS6 Regulates the Biogenesis of Weibel-Palade Body in Endothelial Cells Through Trafficking v-ATPase to Its Limiting Membrane.Frontiers in cell and developmental biology · 2021Article
- Molecular cloning of SLC35D3 and analysis of its role during porcine intramuscular preadipocyte differentiation.BMC genetics · 2020Article
- Gene Expression Signature Predictive of Neuroendocrine Transformation in Prostate Adenocarcinoma.International journal of molecular sciences · 2020Article
- Impact of Brain Insulin Signaling on Dopamine Function, Food Intake, Reward, and Emotional Behavior.Current nutrition reports · 2019Review
- SLC35A5 Protein-A Golgi Complex Member with Putative Nucleotide Sugar Transport Activity.International journal of molecular sciences · 2019Article
- Nucleotide Sugar Transporter SLC35 Family Structure and Function.Computational and structural biotechnology journal · 2019Review
- Active intermixing of indirect and direct neurons builds the striatal mosaic.Nature communications · 2018Article
- Autophagy as an emerging target in cardiorenal metabolic disease: From pathophysiology to management.Pharmacology & therapeutics · 2018Review
- Sorting machineries: how platelet-dense granules differ from α-granules.Bioscience reports · 2018Review
- BLOC-2 subunit HPS6 deficiency affects the tubulation and secretion of von Willebrand factor from mouse endothelial cells.Journal of genetics and genomics = Yi chuan xue bao · 2016Article
- Article
- SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation.Autophagy · 2016Article
Corrections and comments
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Authors and funding
14 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is one of the largest health problems facing the world today. Although twin and family studies suggest about two-thirds of obesity is caused by genetic factors, only a small fraction of this variance has been unraveled. There are still large numbers of genes to be identified that cause variations in body fatness and the associated diseases encompassed in the metabolic syndrome (MetS). A locus near a sequence tagged site (STS) marker D6S1009 has been linked to obesity or body mass index (BMI). However, its genetic entity is unknown. D6S1009 is located in the intergenic region between SLC35D3 and NHEG1. Here we report that the ros mutant mice harboring a recessive mutation in the Slc35d3 gene show obesity and MetS and reduced membrane dopamine receptor D1 (D1R) with impaired dopamine signaling in striatal neurons. SLC35D3 is localized to both endoplasmic reticulum (ER) and early endosomes and interacts with D1R. In ros striatal D1 neurons, lack of SLC35D3 causes the accumulation of D1R on the ER to impair its ER exit. The MetS phenotype is reversible by the administration of D1R agonist to the ros mutant. In addition, we identified two mutations in the SLC35D3 gene in patients with MetS, which alter the subcellular localization of SLC35D3. Our results suggest that the SLC35D3 gene, close to the D6S1009 locus, is a candidate gene for MetS, which is involved in metabolic control in the central nervous system by regulating dopamine signaling.
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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.