Evidence map›Paper›PMID 19002214›Full record

ArticleEuropean journal of human genetics : EJHG2009

MET and autism susceptibility: family and case-control studies.

Inês Sousa, Taane G Clark, Claudio Toma, Kazuhiro Kobayashi, Maja Choma, Richard Holt, Nuala H Sykes, Janine A Lamb, Anthony J Bailey, Agatino Battaglia and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. HGF and MET: From Brain Development to Neurological Disorders.Frontiers in cell and developmental biology · 2021
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Insulin-Independent GABAA Receptor-Mediated Response in the Barrel Cortex of Mice with Impaired Met Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. MET receptor tyrosine kinase as an autism genetic risk factor.International review of neurobiology · 2013
    Review
  19. Autism risk gene MET variation and cortical thickness in typically developing children and adolescents.Autism research : official journal of the International Society for Autism Research · 2012
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 7 institutions in 3 countries.

Inês SousaWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.
Taane G Clark
Claudio Toma
Kazuhiro Kobayashi
Maja Choma
Richard Holt
Nuala H Sykes
Janine A Lamb
Anthony J Bailey
Agatino Battaglia
Elena Maestrini
Anthony P Monaco
International Molecular Genetic Study of Autism Consortium (IMGSAC)
Centre for Human Genetics · GBUniversity of Oxford · GBUniversity of Bologna · ITFondazione Stella Maris · ITOsaka University · JPUniversity of Manchester · GBWarneford Hospital · GB

Funding

Medical Research Council G0601030Wellcome Trust 075491
6 · The paper itself

Abstract

Autism is a common, severe and highly heritable neurodevelopmental disorder. The International Molecular Genetic Study of Autism Consortium (IMGSAC) genome screen for linkage in affected sib-pair families identified a chromosome 7q susceptibility locus (AUTS1), that has subsequently shown evidence of increased sharing in several independent multiplex samples and in two meta-analyses. Taking into account the location of the MET gene under this linkage peak, and the fact that it has recently been reported to be associated with autism, the gene was further analyzed as a promising autism candidate. The gene encodes a transmembrane receptor tyrosine kinase of the hepatocyte growth factor/scatter factor (HGF/SF). MET is best known as an oncogene, but its signalling also participates in immune function, peripheral organ development and repair, and the development of the cerebral cortex and cerebellum (all of which have been observed earlier as being disregulated in individuals with autism). Here we present a family-based association analysis covering the entire MET locus. Significant results were obtained in both single locus and haplotype approaches with a single nucleotide polymorphism in intron 1 (rs38845, P<0.004) and with one intronic haplotype (AAGTG, P<0.009) in 325 multiplex IMGSAC families and 10 IMGSAC trios. Although these results failed to replicate in an independent sample of 82 Italian trios, the association itself was confirmed by a case-control analysis performed using the Italian cohort (P<0.02). The previously reported positive association of rs1858830 failed to replicate in this study. Overall, our findings provide further evidence that MET may play a role in autism susceptibility.

Indexed as

Autistic DisorderCase-Control StudiesGenetic Predisposition to DiseaseGenotypeHaplotypesHumansPolymorphism, Single NucleotideProto-Oncogene ProteinsProto-Oncogene Proteins c-metReceptors, Growth FactorMET protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-metReceptors, Growth Factor

Identifiers

PMID19002214
PMCPMC2685893
OpenAlexW1979255226

What OpenQuestion holds

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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.