Evidence map›Paper›PMID 42596742›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2026

Identification of the Down Syndrome Critical Region 3 Gene as a Mammalian Cell Size Regulator.

Kazumi Kimura, Masakazu Souda, Ryotaro Mori, Yoshimi Kato, Hiroki Kurahashi, Masashi Asai, Kazuo Yamamoto

Abstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2026. 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. Identification of the Down Syndrome Critical Region 3 Gene as a Mammalian Cell Size Regulator.Genes to cells : devoted to molecular & cellular mechanisms · 2026
    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

7 authors.

Kazumi KimuraDivision of Cell Function Research Support, Biomedical Research Support Center, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.ORCID https://orcid.org/0009-0002-1263-6703
Masakazu SoudaDivision of Cell Function Research Support, Biomedical Research Support Center, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Ryotaro MoriDepartment of Genome-Based Drug Discovery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.ORCID https://orcid.org/0009-0004-1761-1892
Yoshimi KatoDivision of Molecular Genetics, Center for Medical Sciences, Fujita Health University, Aichi, Japan.
Hiroki KurahashiDivision of Molecular Genetics, Center for Medical Sciences, Fujita Health University, Aichi, Japan.ORCID https://orcid.org/0000-0002-5690-5218
Masashi AsaiDepartment of Genome-Based Drug Discovery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.ORCID https://orcid.org/0000-0001-6392-0910
Kazuo YamamotoDivision of Cell Function Research Support, Biomedical Research Support Center, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.ORCID https://orcid.org/0000-0002-7633-204X

Funding

Japan Research Society for Adults with Down Syndrome
6 · The paper itself

Abstract

Using a genetic screening approach based on an inducible gene-activating system and cell sorting, Down syndrome critical region 3 (DSCR3) was isolated as a gene whose overexpression increased cell size. Fibroblasts derived from individuals with Down syndrome (DS) exhibit elevated DSCR3 expression at both the mRNA and protein levels, correlating with increased cell volume compared to fibroblasts from healthy donors. Despite a slower proliferation rate, DS fibroblasts demonstrate higher basal and maximal mitochondrial respiration, suggesting enhanced metabolic activity associated with increased cell size. siRNA-mediated knockdown of DSCR3 reduces cell size in both DS and normal fibroblasts, indicating its general role in cell size regulation. As DSCR3 is a component of the retriever complex involved in endosomal cargo recycling, these findings position membrane protein trafficking as a novel module for cell size control.

Indexed as

Cell SizeDown SyndromeAnimalsCell ProliferationFibroblastsHumansMitochondriaProtein Transportcell size regulationDown syndrome critical region genemembrane protein trafficking

Identifiers

PMID42596742
PMCPMC13473892

What OpenQuestion holds

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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.