ArticleJournal of inherited metabolic disease2011
The sodium-dependent di- and tricarboxylate transporter, NaCT, is not responsible for the uptake of D-, L-2-hydroxyglutarate and 3-hydroxyglutarate into neurons.
Article in Journal of inherited metabolic disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Molecular mechanisms mediating relapse following ivosidenib monotherapy in IDH1-mutant relapsed or refractory AML.Blood advances · 2020Article
- Inborn errors of metabolite repair.Journal of inherited metabolic disease · 2020Review
- Mutations in the Na(+)/citrate cotransporter NaCT (SLC13A5) in pediatric patients with epilepsy and developmental delay.Molecular medicine (Cambridge, Mass.) · 2016Article
- Mitochondrial Citrate Transporter-dependent Metabolic Signature in the 22q11.2 Deletion Syndrome.The Journal of biological chemistry · 2015Article
- Article
- Autophagy and oxidative stress in gliomas with IDH1 mutations.Acta neuropathologica · 2014Article
- Sodium-coupled dicarboxylate and citrate transporters from the SLC13 family.Pflugers Archiv : European journal of physiology · 2014Review
- What do we know about IDH1/2 mutations so far, and how do we use it?Acta neuropathologica · 2013Review
- The Role of INDY in Metabolic Regulation.Computational and structural biotechnology journal · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Concentrations of glutarate (GA) and its derivatives such as 3-hydroxyglutarate (3OHGA), D- (D-2OHGA) and L-2-hydroxyglutarate (L-2OHGA) are increased in plasma, cerebrospinal fluid (CSF) and urine of patients suffering from different forms of organic acidurias. It has been proposed that these derivatives cause neuronal damage in these patients, leading to dystonic and dyskinetic movement disorders. We have recently shown that these compounds are eliminated by the kidneys via the human organic anion transporters, OAT1 and OAT4, and the sodium-dependent dicarboxylate transporter 3, NaDC3. In neurons, where most of the damage occurs, a sodium-dependent citrate transporter, NaCT, has been identified. Therefore, we investigated the impact of GA derivatives on hNaCT by two-electrode voltage clamp and tracer uptake studies. None of these compounds induced substrate-associated currents in hNaCT-expressing Xenopus laevis oocytes nor did GA derivatives inhibit the uptake of citrate, the prototypical substrate of hNaCT. In contrast, D- and L-2OHGA, but not 3OHGA, showed affinities to NaDC3, indicating that D- and L-2OHGA impair the uptake of dicarboxylates into astrocytes thereby possibly interfering with their feeding of tricarboxylic acid cycle intermediates to neurons.
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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.