Evidence map›Paper›PMID 40665149›Full record

ArticleScientific reports2025

Disrupting ZBTB7A or BCL11A binding sites reactivates fetal hemoglobin in erythroblasts from healthy and β

Chokdee Wongborisuth, Pawarit Innachai, Chonticha Saisawang, Alisa Tubsuwan, Natee Jearawiriyapaisarn, Pavita Kaewprommal, Jittima Piriyapongsa, Wararat Chiangjong, Usanarat Anurathapan, Duantida Songdej and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026
    Review
  2. Article
  3. Review
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

12 authors.

Chokdee WongborisuthOffices of Health Science Research, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Pawarit InnachaiOffices of Health Science Research, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Chonticha SaisawangCenter for Advanced Therapeutics, Institute of Molecular Biosciences, Mahidol University, Salaya Campus, Nakhon Pathom, 73170, Thailand.
Alisa TubsuwanCenter for Advanced Therapeutics, Institute of Molecular Biosciences, Mahidol University, Salaya Campus, Nakhon Pathom, 73170, Thailand.
Natee JearawiriyapaisarnThalassemia Research Center, Institute of Molecular Biosciences, Mahidol University, Nakhon Pathom, 73170, Thailand.
Pavita KaewprommalNational Biobank of Thailand, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, 12120, Thailand.
Jittima PiriyapongsaNational Biobank of Thailand, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, 12120, Thailand.
Wararat ChiangjongPediatric Translational Research Unit, Department of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Usanarat AnurathapanDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Duantida SongdejDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.
Amornrat TangprasittipapOffices of Health Science Research, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand. tamornrat01@gmail.com.
Suradej HongengDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand.

Funding

Basic Research Fund: the fiscal year 2022 , Mahidol University Grant ID: BRF1-016/2565Faculty of Medicine Ramathibodi Hospital, Mahidol University Grant ID: RF_64041Mahidol University Grant ID: MRC-IM 02/2565
6 · The paper itself

Abstract

CRISPR/Cas9 genome editing has emerged as a promising treatment for genetic diseases like β-thalassemia. Editing γ-globin promoters to disrupt ZBTB7A/LRF or BCL11A binding sites has shown potential for reactivating fetal hemoglobin and treating sickle cell disease. However, its application to β

Indexed as

beta-ThalassemiaCarrier ProteinsDNA-Binding ProteinsErythroblastsFetal HemoglobinHemoglobin ENuclear ProteinsTranscription FactorsBinding SitesCRISPR-Cas Systemsgamma-GlobinsGene EditingHematopoietic Stem CellsHumansPromoter Regions, GeneticRepressor ProteinsBCL11A protein, humanCarrier ProteinsDNA-Binding ProteinsFetal Hemoglobingamma-GlobinsHemoglobin ENuclear ProteinsRepressor ProteinsTranscription FactorsZBTB7A protein, humanBCL11ACRISPR/Cas9 genome editingFetal hemoglobin reactivationZBTB7A/LRFβ0-thalassemia/HbEγ-globin promoter

Identifiers

PMID40665149
PMCPMC12264176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.