Evidence map›Paper›PMID 41402306›Full record

ArticleNature communications2025

Molecular insights into ago-allosteric modulation at cysteinyl leukotriene receptor 2.

Mu Li, Xiaoling Bao, Wanbiao Chen, Yusheng Guo, Xiaomin Mao, Miaofang Xiao, Siqi Liu, Jiawei Li, Limin Zhao, Tiancai Chang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. 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

13 authors.

Mu Li *The Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Xiaoling Bao *Scientific Research Center of Guangzhou Medical University, Guangzhou, Guangdong, China.
Wanbiao Chen *Center for Human Tissues and Organs Degeneration, Faculty of Pharmaceutical Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Yusheng Guo *The Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-5826-299X
Xiaomin Mao *The Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Miaofang Xiao *The Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Siqi LiuThe Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Jiawei LiCenter for Human Tissues and Organs Degeneration, Faculty of Pharmaceutical Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Limin ZhaoDepartment of Geriatric Medicine, Shenzhen Longhua District Central Hospital, Shenzhen, Guangdong, China.
Tiancai ChangThe Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Fumei ZhongThe Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China.
Chongyuan WangCenter for Human Tissues and Organs Degeneration, Faculty of Pharmaceutical Sciences, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China. cy.wang@siat.ac.cn.ORCID http://orcid.org/0000-0001-7477-5376
Heng LiuThe Affiliated Traditional Chinese Medicine Hospital, GMU-GIBH Joint School of Life Sciences, The Guangdong-Hong Kong-Macao Joint Laboratory for Cell Fate Regulation and Diseases, Guangzhou Medical University, Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, State Key Laboratory of Respiratory Disease, Guangzhou, Guangdong, China. 2022991053@gzhmu.edu.cn.ORCID http://orcid.org/0000-0003-2654-4287

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cysteinyl leukotriene receptor CysLT2R, which is activated by the endogenous cysteinyl leukotrienes (CysLTs) LTC4, LTD4, and LTE4, has emerged as a potential therapeutic target due to the involvement in various inflammatory diseases. Accumulating evidence indicates that CysLT2R is also involved in the pathogenesis of cardiovascular diseases and contribute to tumor progression in cancer. However, the structural basis underlying the ligand recognition and the receptor activation remains to be elucidated. Here, we present two cryo-electron microscopy (cryo-EM) structures of the human CysLT2R-G

Indexed as

Receptors, LeukotrieneAllosteric RegulationBinding SitesCryoelectron MicroscopyHEK293 CellsHumansLeukotriene C4Leukotriene D4Models, MolecularProtein BindingSignal Transductioncysteinyl leukotriene receptor 2Leukotriene C4Leukotriene D4Receptors, Leukotriene

Identifiers

PMID41402306
PMCPMC12830604

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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.