Evidence map›Paper›PMID 21653829›Full record

ArticleScience translational medicine2011

Protein interactome reveals converging molecular pathways among autism disorders.

Yasunari Sakai, Chad A Shaw, Brian C Dawson, Diana V Dugas, Zaina Al-Mohtaseb, David E Hill, Huda Y Zoghbi

Abstract read
In one paragraph

Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

136 citing papers in PubMed, 230 citations in OpenAlex.

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  19. International journal of molecular sciences · 2023
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76 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Yasunari SakaiHoward Hughes Medical Institute, Department of Molecular and Human Genetics, Baylor College of Medicine, and Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX 77030, USA.
Chad A Shaw
Brian C Dawson
Diana V Dugas
Zaina Al-Mohtaseb
David E Hill
Huda Y Zoghbi
Baylor College of Medicine · USHarvard University · US

Funding

MOLECULAR PATHOGENESIS STUDIES OF RETT SYNDROMER01NS057819 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 2006 to 2025
$7.5M
Howard Hughes Medical InstituteNINDS NIH HHS R01 NS057819
6 · The paper itself

Abstract

To uncover shared pathogenic mechanisms among the highly heterogeneous autism spectrum disorders (ASDs), we developed a protein interaction network that identified hundreds of new interactions among proteins encoded by ASD-associated genes. We discovered unexpectedly high connectivity between SHANK and TSC1, previously implicated in syndromic autism, suggesting that common molecular pathways underlie autistic phenotypes in distinct syndromes. ASD patients were more likely to harbor copy number variations that encompass network genes than were control subjects. We also identified, in patients with idiopathic ASD, three de novo lesions (deletions in 16q23.3 and 15q22 and one duplication in Xq28) that involve three network genes (NECAB2, PKM2, and FLNA). The protein interaction network thus provides a framework for identifying causes of idiopathic autism and for understanding molecular pathways that underpin both syndromic and idiopathic ASDs.

Indexed as

AnimalsBrainCell LineChild Development Disorders, PervasiveHumansImmunoprecipitationInfant, NewbornMiceNerve Tissue ProteinsProtein Interaction MappingTwo-Hybrid System TechniquesNerve Tissue Proteins

Identifiers

PMID21653829
PMCPMC3169432
OpenAlexW2126924893

What OpenQuestion holds

Textmetadata
LicenceTDM
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.