Evidence map›Paper›PMID 41354902›Full record

ArticleCellular & molecular immunology2026

MST1 bridges LYN and SHP-1 to suppress FcεRI-mediated mast cell activation and allergic responses.

Mengyao Li, Huihan Li, Wenlong Lin, Lin Tong, Lingman Dai, Qiannan Zhao, Mengting Hu, Zhimin Chen, Yiting Zhou, Qingqing Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 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

11 authors.

Mengyao Li *Department of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Huihan Li *Department of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Wenlong LinInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Lin TongDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Lingman DaiDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Qiannan ZhaoDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Mengting HuDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Zhimin ChenDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Yiting ZhouLiangzhu Laboratory, Zhejiang University Medical Center, Hangzhou, China. zhouyt@zju.edu.cn.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China. wqq@zju.edu.cn.ORCID 0000-0002-0415-0052
Yuanyuan ZhangDepartment of Pulmonology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China. chzyy@zju.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 8187060308National Natural Science Foundation of China (National Science Foundation of China) U22A20307, 81930041Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LZ24H100001
6 · The paper itself

Abstract

Mammalian sterile-20-like kinase 1 (MST1) is a core component of the Hippo signaling pathway. A previous study of 24 patients with MST1 deficiency revealed that more than half of the patients presented symptoms of airway hyperresponsiveness and atopic dermatitis. We also found significantly reduced MST1 expression in patients with allergies and in mouse models of allergic asthma, suggesting that aberrant MST1 expression may be broadly relevant to allergic diseases. However, the specific mechanism by which MST1 may be related to allergic disorders has remained unclear. In our study, Mst1

Indexed as

HypersensitivityMast CellsProtein Serine-Threonine KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6Proto-Oncogene ProteinsReceptors, IgEsrc-Family KinasesAnimalsAsthmaCell DegranulationHepatocyte Growth FactorHippo KinasesHumansImmunoglobulin EMiceMice, Inbred C57BLHepatocyte Growth FactorHippo KinasesImmunoglobulin Elyn protein-tyrosine kinaseProtein Serine-Threonine KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6Proto-Oncogene ProteinsPtpn6 protein, mouseReceptors, IgEsrc-Family KinasesStk4 protein, mouseAllergic diseaseFcεRI signalingLCK/YES-related protein tyrosine kinaseMammalian sterile 20-like kinase 1Mast cellSRC homology domain-containing tyrosine phosphatase-1

Identifiers

PMID41354902
PMCPMC12753851

What OpenQuestion holds

Textmetadata
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.