Evidence map›Paper›PMID 39390489›Full record

ArticleClinical genetics2025

A Strong Candidate Gene for Nonsyndromic Intellectual Disability Phenotype: SGSM3.

Ayberk Turkyilmaz, Kubra Adanur Saglam, Mustafa Yilmaz, Alper Han Cebi

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In one paragraph

Article in Clinical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

4 authors.

Ayberk TurkyilmazDepartment of Medical Genetics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.
Kubra Adanur SaglamDepartment of Medical Genetics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.ORCID 0000-0003-0201-6877
Mustafa YilmazDepartment of Medical Genetics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.ORCID 0009-0002-0134-3999
Alper Han CebiDepartment of Medical Genetics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SGSM proteins are small modulator proteins interacting with proteins in the RAS signaling pathway. Studies with mouse and human tissues indicated that SGSM genes were highly expressed in the brain and could be expressed at different levels at different stages of development in fetal and adult brain tissue. It was first reported by Birnbaum et al. that the SGSM3 gene might be associated with a Mendelian inherited disease in families of Ashkenazi Jews with clinical manifestations of intellectual disability (ID). In this study, a novel homozygous stop-gain (NM_015705.6: c.1576C>T: p.(Arg526Ter)) variation was detected in the SGSM3 gene in two siblings with short stature and ID findings. The report of two cases with bi-allelic LOF variants in the SGSM3 gene from different populations with similar clinical manifestations strengthens the potential of this gene as a candidate gene for the nonsyndromic ID phenotype. Functional studies are required to investigate the signaling pathways affected by SGSM3 gene variations to produce the ID phenotype and their effect on the functioning of neurons.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseIntellectual DisabilityHomozygoteHumansMutationPedigreePhenotypecandidate geneintellectual disabilitynovel phenotypeSGSM3

Identifiers

PMID39390489
PMCPMC11725557

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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.