Evidence map›Paper›PMID 40874937›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Tead1a Initiates Transcriptional Priming Through the TEAD1a/YAP-Notch1-Spi1/Cebpα Axis to Promote Neutrophil Fate.

Wang Yiqin, Yang Ruimeng, Wang Peihong, Liu Xiaohui, Yuan Hao, Huang Hongli, Zhou Yongjian, Xie Baoshu

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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
–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

5 citing papers in PubMed.

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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

8 authors.

Wang YiqinDepartment of Gastroenterology and Hepatology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, 510080, China.
Yang RuimengCNRS-LIA Hematology and Cancer, Sino-French Research Center for Life Sciences and Genomics, State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200000, China.
Wang PeihongDepartment of Hematology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, 510080, China.
Liu XiaohuiCNRS-LIA Hematology and Cancer, Sino-French Research Center for Life Sciences and Genomics, State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200000, China.
Yuan HaoCNRS-LIA Hematology and Cancer, Sino-French Research Center for Life Sciences and Genomics, State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200000, China.
Huang HongliDepartment of Gastroenterology and Hepatology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, 510080, China.
Zhou YongjianDepartment of Gastroenterology and Hepatology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, 510080, China.
Xie BaoshuDepartment of Neurosurgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.ORCID https://orcid.org/0000-0002-0684-5341

Funding

Guangdong Province Science and Technology Department's Guangdong-Hong Kong-Macao Joint Innovation Program 2023A0505010007Medical Science Research Project in Guangdong B2025093National Natural Science Foundation of China NSFC 82100124Specific Research Project of Guangxi for Research Bases and Talents 2025A03J4148
6 · The paper itself

Abstract

Clinical neutropenia, a blood disorder marked by faulty neutrophil production, resists effective treatment due to developmental bottlenecks in granulopoiesis. While the current therapy, such as granulocyte colony-stimulating factor (G-CSF), boosts neutrophil counts, its late-stage action mobilizes dysfunctional cells, underscoring the need for early-lineage therapeutic interventions. Leveraging zebrafish models, we found that transcriptional enhanced associate domain 1a (TEAD1a) initiates transcriptional priming to govern neutrophil lineage specification preceding hematopoietic stem cell formation. Genetic ablation of TEAD1a or disruption of its interaction with Yes-associated protein 1 (YAP1) induces profound neutropenia. Mechanistic interrogation reveals that TEAD1a/YAP1 complexes potentiate Notch1-mediated signaling to activate a Spi1/Cebpα transcriptional cascade during myeloid progenitor specification. This study uncovers a novel developmental regulatory window for myeloid lineage commitment and demonstrates the evolutionarily conserved role of TEAD1a-mediated transcriptional priming in orchestrating neutrophil development. The discovery of this ultra-early regulatory node provides a molecularly defined target for generating developmentally competent neutrophils, offering an innovative therapeutic strategy for refractory neutropenia.

Indexed as

DNA-Binding ProteinsNeutrophilsTranscription FactorsAdaptor Proteins, Signal TransducingAnimalsCCAAT-Enhancer-Binding ProteinsHumansNeutropeniaProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptor, Notch1Signal TransductionTEA Domain Transcription FactorsTrans-ActivatorsYAP-Signaling ProteinsZebrafishAdaptor Proteins, Signal TransducingCCAAT-Enhancer-Binding ProteinsDNA-Binding ProteinsProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptor, Notch1TEA Domain Transcription FactorsTrans-ActivatorsTranscription FactorsYAP-Signaling ProteinsZebrafish Proteinsdevelopmental hematopoiesisneutropeniasingle‐cell sequencingTEAD1atranscriptional priming

Identifiers

PMID40874937
PMCPMC12591127

What OpenQuestion holds

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Registered trials

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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.