Evidence map›Paper›PMID 41927540›Full record

ArticleNature communications2026

MYC-induced USP10 stabilizes SOX4 to promote thymocyte proliferation and leukemia onset in mice.

Mengdi Zhang, Hanrui Wu, Xiaoxi Lin, Fan Zhao, Qiaolin Deng, Linrong Lu, Xia Li, Xiang Chen, Hong Liu, Paul E Love and 2 more

Abstract read
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.

Mengdi Zhang *National Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0001-5752-9464
Hanrui Wu *National Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Xiaoxi Lin *National Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-0358-3972
Fan ZhaoInstitute of Immunology and Department of Rheumatology at Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Qiaolin DengDepartment of Physiology and Pharmacology, Karolinska Institute, Solna, Sweden.ORCID http://orcid.org/0000-0001-5934-7816
Linrong LuInstitute of Immunology and Department of Rheumatology at Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0002-0171-4115
Xia LiNational Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0001-8665-7983
Xiang ChenFurong Laboratory, Changsha, Hunan, China.ORCID http://orcid.org/0000-0001-8187-636X
Hong LiuFurong Laboratory, Changsha, Hunan, China. hongliu1014@csu.edu.cn.ORCID http://orcid.org/0000-0001-9976-2985
Paul E LoveSection on Hematopoiesis and Lymphocyte Biology, Eunice Kennedy Shriver, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. lovep@mail.nih.gov.ORCID http://orcid.org/0000-0002-6682-7372
Jiaqi HuangNational Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China. Jiaqi.huang@live.com.ORCID http://orcid.org/0000-0002-7808-9477
Bin ZhaoNational Clinical Research Center for Endocrine and Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China. binzhao@csu.edu.cn.ORCID http://orcid.org/0000-0003-4302-2333

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82100949National Natural Science Foundation of China (National Science Foundation of China) 82170795National Natural Science Foundation of China (National Science Foundation of China) 82470814National Natural Science Foundation of China (National Science Foundation of China) 82470931
6 · The paper itself

Abstract

Dysregulation of thymic T cell development compromises immune homeostasis and can lead to leukemic transformation, but the molecular mechanisms linking developmental signals, proliferative cues, and leukemogenesis remain incompletely understood. Here, we integrate deubiquitinase library screening and publicly available single-cell RNA sequencing to analyze mouse and human thymocytes. We find the deubiquitinase USP10 to be expressed in thymocytes, and also elevated in peripheral blood from patients with T-cell acute lymphoblastic leukemia (T-ALL) compared to healthy controls; by contrast, T cell-specific USP10 deficiency blocks mouse thymocyte proliferation and differentiation. Mechanistically, USP10 interacts with SOX4, de-ubiquitinating and protecting SOX4 from degradation to promote thymocyte proliferation, with SOX4 overexpression restoring thymocyte differentiation in USP10-deficient mice. Lastly, MYC induces Usp10 expression, and pharmacologic inhibition of USP10 delays MYC-driven leukemogenesis in a mouse leukemia model. Our results thus identify USP10 as coordinator of developmental signals and oncogenic processes in thymocytes, and implicate USP10 as a potential target for T-ALL therapy.

Indexed as

Precursor T-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-mycSOXC Transcription FactorsThymocytesUbiquitin ThiolesteraseAnimalsCell DifferentiationCell ProliferationHumansMiceMice, Inbred C57BLMice, KnockoutUbiquitinationMyc protein, mouseProto-Oncogene Proteins c-mycSOX4 protein, humanSox4 protein, mouseSOXC Transcription FactorsUbiquitin ThiolesteraseUSP10 protein, humanUSP10 protein, mouse

Identifiers

PMID41927540
PMCPMC13216311

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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.