Evidence map›Paper›PMID 39709321›Full record

ArticleCellular and molecular life sciences : CMLS2024

SHIP-1 regulates the differentiation and function of Tregs via inhibiting mTORC1 activity.

Zuochen Du, Jinzhi Wang, Qian Liu, Di Yang, Xiaoyu Sun, Lu Huang, Pei Huang, Xingye Tang, Heather Miller, Lisa Westerberg and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2024. 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. The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    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

14 authors.

Zuochen Du *Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Jinzhi Wang *Chongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Qian Liu *Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Di YangChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Xiaoyu SunChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Lu HuangChongqing Key Laboratory of Child Infection and Immunity, Children's Hospital of Chongqing Medical University, Chongqing, China.
Pei HuangThe Department of Pediatrics, Affiliated Hospital of Zunyi Medical University, Guizhou Children's Hospital, Zunyi, Guizhou Province, China.
Xingye TangDepartment of Otolaryngology, Children's Hospital of Chongqing Medical University, Chongqing, China.
Heather MillerThe Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Lisa WesterbergDepartment of Microbiology Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Yoshimura AkihikoDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.
Lu YangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Xingrong DuShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, China.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. chaohongliu80@126.com.ORCID http://orcid.org/0000-0001-7028-4625

Funding

National Natural Science Foundation of China 32100710National Natural Science Foundation of China 32360184
6 · The paper itself

Abstract

Cell metabolism is crucial for orchestrating the differentiation and function of regulatory T cells (Tregs). However, the underlying mechanism that coordinates cell metabolism to regulate Treg activity is not completely understood. As a pivotal molecule in lipid metabolism, the role of SHIP-1 in Tregs remains unknown. In this study, we found SHIP-1 Treg KO mice (SHIP-1 specifically deleted in regulatory T cells) had severe autoimmunity with increased Tregs in the thymus and disrupted peripheral T cell homeostasis. Mechanistically, CD4

Indexed as

Cell DifferentiationMechanistic Target of Rapamycin Complex 1Mice, KnockoutPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesSignal TransductionT-Lymphocytes, RegulatoryAnimalsAutoimmunityMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesSirolimusMechanistic Target of Rapamycin Complex 1Phosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesSirolimusCell metabolismmTORSHIP-1Treg cells

Identifiers

PMID39709321
PMCPMC11663208

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.