Evidence map›Paper›PMID 42831136›Full record

ArticleJournal of structural biology: X2026

Investigating the effects of missense mutations on the dual Ras/Rap activation mechanism of SYNGAP1 using molecular modelling.

Aliaa E Ali, Arto Liljeblad, Jukka V Lehtonen, Noboru H Komiyama, Pekka A Postila

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of structural biology: X, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Aliaa E AliInstitute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland.
Arto LiljebladInstitute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland.
Jukka V LehtonenStructural Bioinformatics Laboratory, Department of Natural and Health Sciences, Åbo Akademi University, FI-20500 Turku, Finland.
Noboru H KomiyamaInstitute for Neuroscience and Cardiovascular Research, University of Edinburgh, Edinburgh EH16 4SB, UK.
Pekka A PostilaInstitute of Biomedicine, Integrative Physiology and Pharmacology, University of Turku, FI-20014 Turku, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SynGAP (Synaptic GTPase-Activating Protein) is enriched in the postsynaptic density, where it accelerates GTP hydrolysis by Ras- and Rap-GTPases. In forebrain, SynGAP is essential for synaptic plasticity and cognitive development, and de novo mutations in Author summary: We study SynGAP, a protein essential for how brain cells communicate, learn, and develop. Changes in the

Indexed as

Activation mechanismBinding free energy calculationsIntellectual disabilityMissense mutationMolecular dynamics (MD) simulationsRap1b-GTPaseRas-GTPaseSynGAPSYNGAP1SynGAP-related disorder (SRD)Tumor suppressor

Identifiers

PMID42831136
PMCPMC13634398

What Socratic holds

Textmetadata
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 Socratic graph.