Evidence map›Paper›PMID 28420080›Full record

ReviewInternational journal of molecular sciences2017

Delineating the Common Biological Pathways Perturbed by ASD's Genetic Etiology: Lessons from Network-Based Studies.

Oded Oron, Evan Elliott

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. The involvement of the canonical Wnt-signaling receptor LRP5 and LRP6 gene variants with ADHD and sexual dimorphism: Association study and meta-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
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  16. Bio-collections in autism research.Molecular autism · 2017
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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

2 authors.

Oded OronMolecular and Behavioral Neurosciences Lab, Bar-Ilan University, Faculty of Medicine, 13215 Safed, Israel. odedoron@gmail.com.
Evan ElliottMolecular and Behavioral Neurosciences Lab, Bar-Ilan University, Faculty of Medicine, 13215 Safed, Israel. evan.elliott@biu.ac.il.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent decades it has become clear that Autism Spectrum Disorder (ASD) possesses a diverse and heterogeneous genetic etiology. Aberrations in hundreds of genes have been associated with ASD so far, which include both rare and common variations. While one may expect that these genes converge on specific common molecular pathways, which drive the development of the core ASD characteristics, the task of elucidating these common molecular pathways has been proven to be challenging. Several studies have combined genetic analysis with bioinformatical techniques to uncover molecular mechanisms that are specifically targeted by autism-associated genetic aberrations. Recently, several analysis have suggested that particular signaling mechanisms, including the Wnt and Ca

Indexed as

Genetic Predisposition to DiseaseSignal TransductionAnimalsAutism Spectrum DisorderCalcium SignalingCalmodulinComputational BiologyGene Expression ProfilingHumansMutationProtein BindingProtein Interaction MappingWnt Signaling PathwayCalmodulinASDautismCalciumCalmodulinFragile-X SyndromegeneticsmTORnetworksNGFWnt

Identifiers

PMID28420080
PMCPMC5412412

What OpenQuestion holds

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LicenceCC BY
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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.