Evidence map›Paper›PMID 37708136›Full record

ArticlePloS one2023

Gene regulation analysis of patient-derived iPSCs and its CRISPR-corrected control provides a new tool for studying perturbations of ELMOD3 c.512A>G mutation during the development of inherited hearing loss.

Xianlin Liu, Jie Wen, Xuezhong Liu, Anhai Chen, Sijun Li, Jing Liu, Jie Sun, Wei Gong, Xiaoming Kang, Zhili Feng and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Xianlin LiuDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jie WenDepartment of Otolaryngology Head and Neck Surgery, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Xuezhong LiuDepartment of Otolaryngology, University of Miami Miller School of Medicine, Miami, FL, United States of America.
Anhai ChenDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Sijun LiDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jing LiuDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jie SunDepartment of Otolaryngology Head and Neck Surgery, The Eighth Affiliated Hospital, Sun Yat-sen University, Futian District, Shenzhen, China.
Wei GongDepartment of Otolaryngology Head and Neck Surgery, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Xiaoming KangDepartment of Otolaryngology Head and Neck Surgery, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Zhili FengDepartment of Otolaryngology Head and Neck Surgery, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Chufeng HeDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lingyun MeiDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jie LingMedical Functional Experiment Center, School of Basic Medical Science, Central South University, Changsha, Hunan, China.
Yong FengDepartment of Otolaryngology, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0003-3824-3780
Central South University · CNChangsha Central Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ELMOD3 gene is implicated in causing autosomal recessive/dominant non-syndromic hearing loss in humans. However, the etiology has yet to be completely elucidated. In this study, we generated a patient-derived iPSC line carrying ELMOD3 c.512A>G mutation. In addition, the patient-derived iPSC line was corrected by CRISPR/Cas9 genome editing system. Then we applied RNA sequencing profiling to compare the patient-derived iPSC line with different controls, respectively (the healthy sibling-derived iPSCs and the CRISPR/Cas9 corrected iPSCs). Functional enrichment and PPI network analysis revealed that differentially expressed genes (DEGs) were enriched in the gene ontology, such as sensory epithelial development, intermediate filament cytoskeleton organization, and the regulation of ion transmembrane transport. Our current work provided a new tool for studying how disruption of ELMOD3 mechanistically drives hearing loss.

Indexed as

DeafnessHearing LossInduced Pluripotent Stem CellsGene Expression RegulationGTPase-Activating ProteinsHumansMutationELMOD3 protein, humanGTPase-Activating Proteins

Identifiers

PMID37708136
PMCPMC10501637
OpenAlexW4386737820

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.