Evidence map›Paper›PMID 23251443›Full record

ArticlePloS one2012

Mutation in Parkinson disease-associated, G-protein-coupled receptor 37 (GPR37/PaelR) is related to autism spectrum disorder.

Eriko Fujita-Jimbo, Zhi-Ling Yu, Hong Li, Takanori Yamagata, Masato Mori, Takashi Momoi, Mariko Y Momoi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Inflammation and Infection in Pain and the Role of GPR37.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. GPR37 is processed in the N-terminal ectodomain by ADAM10 and furin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Protective effects of GPR37FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Article
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

7 authors at 4 institutions in 3 countries.

Eriko Fujita-JimboDepartment of Pediatrics, Jichi Medical University, Yakushiji, Shimotsukeshi, Tochigi, Japan.
Zhi-Ling Yu
Hong Li
Takanori Yamagata
Masato Mori
Takashi Momoi
Mariko Y Momoi
Jichi Medical University · JPChina Medical University · CNInternational University of Health and Welfare · JPMichigan United · US

Funding

Genomewide Search--Autism Susceptibility Loci-supplementR01MH064547 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GESCHWIND, DANIEL H · 2002 to 2006
$9.6M
NIMH NIH HHS MH64547NIMH NIH HHS R01 MH064547
6 · The paper itself

Abstract

Little is known about the molecular pathogenesis of Autism spectrum disorder (ASD), a neurodevelopmental disorder. Here we identified two mutations in the G-protein-coupled receptor 37 gene (GPR37) localized on chromosome 7q31-33, called the AUTS1 region, of ASD patients; 1585-1587 ttc del (Del312F) in one Japanese patient and G2324A (R558Q) in one Caucasian patient. The Del312F was located in the conserved transmembrane domain, and the R558Q was located in a conserved region just distal to the last transmembrane domain. In addition, a potential ASD-related GPR37 variant, T589M, was found in 7 affected Caucasian men from five different families. Our results suggested that some alleles in GPR37 were related to the deleterious effect of ASD. GPR37 is associated with the dopamine transporter to modulate dopamine uptake, and regulates behavioral responses to dopaminergic drugs. Thus, dopaminergic neurons may be involved in the ASD. However, we also detected the Del321F mutation in the patient's unaffected father and R558Q in not only an affected brother but also an unaffected mother. The identification of unaffected parents that carried the mutated alleles suggested that the manifestation of ASD was also influenced by factors other than these mutations, including endoplasmic reticulum stress of the mutated proteins or gender. Our study will provide the new insight into the molecular pathogenesis of ASD.

Indexed as

MutationAdolescentAdultBase SequenceChildChild Development Disorders, PervasiveChild, PreschoolChromosome MappingChromosomes, Human, Pair 7DNA PrimersFemaleHumansMaleMutagenesis, Site-DirectedParkinson DiseasePolymerase Chain ReactionDNA PrimersGPR37 receptor, humanReceptors, G-Protein-Coupled

Identifiers

PMID23251443
PMCPMC3520984
OpenAlexW2165199490

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.