Evidence map›Paper›PMID 42918790›Full record

ArticleNature communications2026

SATB1 lowers the T cell receptor signaling threshold for thymocyte positive selection via super-enhancer reprogramming.

Wei Xue, Keyi Li, Junwei Luo, Delong Feng, Ranran Dai, Yongchang Zhu, Yiting Yang, Litao Qin, Yan Zhang, Jiarui Zhang and 2 more

Abstract read
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In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Wei XueCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-9986-4751
Keyi LiCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Junwei LuoDepartment of Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.
Delong FengDepartment of Dermatology, Hunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-0664-0063
Ranran DaiZhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Yongchang ZhuDepartment of Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, China.ORCID http://orcid.org/0000-0003-0145-455X
Yiting YangCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-3328-5415
Litao QinMedical Genetic Institute of Henan Province, Henan Key Laboratory of Genetic Diseases and Functional Genomics, People's Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.ORCID http://orcid.org/0000-0001-7501-4819
Yan ZhangCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-5735-207X
Jiarui ZhangCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0003-4384-4214
Bo LeiEye Institute, Henan Academy of Innovations in Medical Science, Zhengzhou, China. bolei99@126.com.ORCID http://orcid.org/0000-0002-5497-0905
Bingtao HaoCancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. haobt123@zzu.edu.cn.ORCID http://orcid.org/0000-0003-1997-9338

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32370939
6 · The paper itself

Abstract

In early T cell development, thymocytes undergoing positive selection receive relatively weak T cell receptor (TCR) signals. However, the mechanisms by which thymocytes translate weak and transient TCR signals into lineage-defining transcriptional programs remain unclear. Here, we show that SATB1 plays a key role in enhancer activation during positive selection, as it promotes the expression of positive selection-associated genes by enhancing super-enhancer (SE) activation. Notably, SATB1 deficiency disrupts SE topological organization, weakens promoter-enhancer interactions, blunts TCR-induced Ca

Indexed as

Matrix Attachment Region Binding ProteinsReceptors, Antigen, T-CellSuper EnhancersThymocytesAnimalsCell DifferentiationEnhancer Elements, GeneticMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticSignal TransductionMatrix Attachment Region Binding ProteinsReceptors, Antigen, T-CellSatb1 protein, mouse

Identifiers

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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.