Evidence map›Paper›PMID 26215737›Full record

ArticleAmino acids2015

Hypomorphic variants of cationic amino acid transporter 3 in males with autism spectrum disorders.

Caroline Nava, Johanna Rupp, Jean-Paul Boissel, Cyril Mignot, Agnès Rastetter, Claire Amiet, Aurélia Jacquette, Céline Dupuits, Delphine Bouteiller, Boris Keren and 14 more

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Amino acids, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

24 authors at 10 institutions in 2 countries.

Caroline NavaSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Johanna RuppDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Jean-Paul BoisselDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Cyril MignotDépartement de Génétique et de Cytogénétique, Hôpital de la Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Agnès RastetterSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Claire AmietService de psychiatrie de l'enfant et de l'adolescent, Hôpital Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Aurélia JacquetteDépartement de Génétique et de Cytogénétique, Hôpital de la Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Céline DupuitsSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Delphine BouteillerSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Boris KerenDépartement de Génétique et de Cytogénétique, Hôpital de la Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Merle RubergSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Anne FaudetDépartement de Génétique et de Cytogénétique, Hôpital de la Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Diane DoummarService de neuropédiatrie, Hôpital Trousseau, AP-HP, Paris, France.
Anne PhilippeService de psychiatrie de l'enfant et de l'adolescent, Hôpital Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Didier PérisseService de psychiatrie de l'enfant et de l'adolescent, Hôpital Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Claudine LaurentSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Nicolas LebrunInstitut Cochin, Inserm U567, UMR 8104, Université René Descartes, Paris 5, France.
Vincent GuillemotBioinformatics and Biostatistics Core Facility (iCONICS), Institut du cerveau et de la moelle épinière (ICM), Paris, France.
Jamel ChellyInstitut Cochin, Inserm U567, UMR 8104, Université René Descartes, Paris 5, France.
David CohenService de psychiatrie de l'enfant et de l'adolescent, Hôpital Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Delphine HéronDépartement de Génétique et de Cytogénétique, Hôpital de la Pitié-Salpêtrière, AP-HP, 75013, Paris, France.
Alexis BriceSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France.
Ellen I ClossDepartment of Pharmacology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Christel DepienneSorbonne Universités, UPMC Univ Paris 06, UMR S 1127, ICM, 75013, Paris, France. christel.depienne@upmc.fr.
Pitié-Salpêtrière Hospital · FRCentre National de la Recherche Scientifique · FRAssistance Publique – Hôpitaux de Paris · FRSorbonne Université · FRInserm · FRJohannes Gutenberg University Mainz · DECentre d'Épidémiologie sur les Causes Médicales de Décès · FRInstitut Cochin · FRInstitut du Cerveau · FRUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cationic amino acid transporters (CATs) mediate the entry of L-type cationic amino acids (arginine, ornithine and lysine) into the cells including neurons. CAT-3, encoded by the SLC7A3 gene on chromosome X, is one of the three CATs present in the human genome, with selective expression in brain. SLC7A3 is highly intolerant to variation in humans, as attested by the low frequency of deleterious variants in available databases, but the impact on variants in this gene in humans remains undefined. In this study, we identified a missense variant in SLC7A3, encoding the CAT-3 cationic amino acid transporter, on chromosome X by exome sequencing in two brothers with autism spectrum disorder (ASD). We then sequenced the SLC7A3 coding sequence in 148 male patients with ASD and identified three additional rare missense variants in unrelated patients. Functional analyses of the mutant transporters showed that two of the four identified variants cause severe or moderate loss of CAT-3 function due to altered protein stability or abnormal trafficking to the plasma membrane. The patient with the most deleterious SLC7A3 variant had high-functioning autism and epilepsy, and also carries a de novo 16p11.2 duplication possibly contributing to his phenotype. This study shows that rare hypomorphic variants of SLC7A3 exist in male individuals and suggest that SLC7A3 variants possibly contribute to the etiology of ASD in male subjects in association with other genetic factors.

Indexed as

Amino Acid SequenceAmino Acid Transport Systems, BasicAnimalsAutism Spectrum DisorderBiotinylationBrainCationic Amino Acid Transporter 1Cell MembraneChildChromosomes, Human, XEpilepsyGene FrequencyHumansLoss of HeterozygosityMaleMolecular ConformationAmino Acid Transport Systems, BasicCationic Amino Acid Transporter 1SLC7A3 protein, humanAutism spectrum disordersCationic amino acid transporterChromosome XExome sequencingOligogenism

Identifiers

PMID26215737
PMCPMC4633447
OpenAlexW966012335

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Registered trials

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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.