Evidence map›Paper›PMID 30443311›Full record

ArticleMolecular autism2018

Loss of the Chr16p11.2 ASD candidate gene

Denise Haslinger, Regina Waltes, Afsheen Yousaf, Silvia Lindlar, Ines Schneider, Chai K Lim, Meng-Miao Tsai, Boyan K Garvalov, Amparo Acker-Palmer, Nicolas Krezdorn and 6 more

Open access · goldAbstract read
In one paragraph

Article in Molecular autism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Nutrients · 2022
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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

16 authors at 5 institutions in 3 countries.

Denise Haslinger1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Regina Waltes1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Afsheen Yousaf1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Silvia Lindlar1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Ines SchneiderInstitute of Experimental Cancer Research in Pediatrics, Frankfurt am Main, Germany.
Chai K Lim3Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales Australia.
Meng-Miao Tsai4Neuropathology, University of Giessen, Giessen, Germany.
Boyan K Garvalov4Neuropathology, University of Giessen, Giessen, Germany.
Amparo Acker-Palmer6Institute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), JW Goethe University of Frankfurt, Frankfurt am Main, Germany.
Nicolas Krezdorn7GenXPro GmbH, Frankfurt am Main, Germany.
Björn Rotter7GenXPro GmbH, Frankfurt am Main, Germany.
Till Acker4Neuropathology, University of Giessen, Giessen, Germany.
Gilles J Guillemin3Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales Australia.
Simone FuldaInstitute of Experimental Cancer Research in Pediatrics, Frankfurt am Main, Germany.
Christine M Freitag1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.
Andreas G Chiocchetti1Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, JW Goethe University Frankfurt, Frankfurt am Main, Germany.ORCID 0000-0002-7329-9985
Goethe University Frankfurt · DEJustus-Liebig-Universität Gießen · DEGenXPro (Germany) · DEInstitute of Clinical Cancer Research · DEMacquarie University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Altered neuronal development is discussed as the underlying pathogenic mechanism of autism spectrum disorders (ASD). Copy number variations of 16p11.2 have recurrently been identified in individuals with ASD. Of the 29 genes within this region, Methods: The gene dosage-dependent change of Results: Conclusions: In this study,

Indexed as

Autism Spectrum DisorderCell DifferentiationCell Line, TumorChromosome DeletionChromosomes, Human, Pair 16DNA Copy Number VariationsHumansNeuronsNicotinate-Nucleotide Diphosphorylase (Carboxylating)PentosyltransferasesNicotinate-Nucleotide Diphosphorylase (Carboxylating)Pentosyltransferases16p11.2AutismCRISPR/Cas9KynurenineQuinolinate phosphoribosyltransferaseQuinolinic acidSholl analysis

Identifiers

PMID30443311
PMCPMC6220561
OpenAlexW2900361247

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.