Evidence map›Paper›PMID 40404920›Full record

ArticleCell death and differentiation2025

Thymic egress and peripheral T cell homeostasis regulated by Rho GTPase-activating protein 30.

Huiling Zhang, Zhihan Guo, Jingjing Yi, Jiaying Wu, Yihan Wang, Tingrong Ren, Yuqi Zhang, Haiping Zhao, Nana Wu, Gaigai Wei and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

11 authors.

Huiling ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.ORCID 0000-0002-5981-2404
Zhihan GuoChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jingjing YiChildren's Hospital of Fudan University, National Children's Medical Center, Fudan University, Shanghai, China.
Jiaying WuChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yihan WangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Tingrong RenChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yuqi ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Haiping ZhaoChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Nana WuChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Gaigai WeiChildren's Hospital of Fudan University, National Children's Medical Center, Fudan University, Shanghai, China.
Duanwu ZhangChildren's Hospital of Fudan University, National Children's Medical Center, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, China. duanwu@fudan.edu.cn.ORCID 0000-0003-2946-846X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32370926National Natural Science Foundation of China (National Science Foundation of China) 82071780Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 20ZR1407600Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 21JC1400900
6 · The paper itself

Abstract

T cells are central to adaptive immunity, with proper thymic development and egress critical for T cell homeostasis in peripheral tissues. The molecular mechanisms governing thymic egress remain poorly understood. Here, we identify Rho GTPase-activating protein 30 (ARHGAP30), predominantly expressed in lymphoid organs and previously uncharacterized in immunity, as a key regulator of thymocyte migration and egress. Loss of ARHGAP30 leads to impaired thymic development and severe T cell lymphopenia. Notably, Arhgap30-deficient mice exhibit a reduced number of immature single-positive (SP) thymocytes but a normal number of mature SP thymocytes, indicating a blockade in thymic egress. Mechanistically, ARHGAP30 deficiency lowers GTP-bound active RAC1 independent of its GAP activity, impairing actin polarization and thymocyte motility. ARHGAP30 selectively binds and stabilizes active RAC1, preventing its proteasomal degradation via K48-linked ubiquitination. These findings establish ARHGAP30 as a critical checkpoint for thymic egress and underscore its essential role in maintaining peripheral T cell homeostasis.

Indexed as

GTPase-Activating ProteinsHomeostasisThymus GlandT-LymphocytesAnimalsCell MovementHumansMiceMice, Inbred C57BLMice, Knockoutrac1 GTP-Binding ProteinThymocytesUbiquitinationGTPase-Activating Proteinsrac1 GTP-Binding Protein

Identifiers

PMID40404920
PMCPMC12669708

What OpenQuestion holds

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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.