Evidence map›Paper›PMID 27811945›Full record

ArticleCell research2016

Scaffolding protein Gab1 regulates myeloid dendritic cell migration in allergic asthma.

Yun Zhang, Yun Xu, Shuwan Liu, Xiaohong Guo, Dong Cen, Jiaqi Xu, Heyuan Li, Kaijun Li, Chunlai Zeng, Linrong Lu and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 23% of its field
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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  17. Gab1, a therapeutic target for allergic asthma?Journal of Xiangya medicine · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 1 country.

Yun ZhangDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Yun XuDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Shuwan LiuDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Xiaohong GuoDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Dong CenDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Jiaqi XuDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Heyuan LiDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Kaijun LiLishui Central Hospital, Affiliated Lishui Hospital of Zhejiang University, Lishui, Zhejiang 323000, China.
Chunlai ZengLishui Central Hospital, Affiliated Lishui Hospital of Zhejiang University, Lishui, Zhejiang 323000, China.
Linrong LuThe Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Yiting ZhouDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Huahao ShenDepartment of Respiratory and Critical Care Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Hongqiang ChengDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Xue ZhangDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Yuehai KeDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China.
Zhejiang University · CNLishui Central Hospital · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a common allergic disorder involving a complex interplay among multiple genetic and environmental factors. Recent studies identified genetic variants of human GAB1 as a novel asthma susceptibility factor. However, the functions of Gab1 in lung remain largely unexplored. In this study, we first observed an elevation of Gab1 level in peripheral blood mononuclear cells from asthmatic patients during acute exacerbation compared with convalescence. Mice with a selectively disrupted Gab1 in myeloid dendritic cells (mDCs) considerably attenuated allergic inflammation in experimental models of asthma. Further investigations revealed a prominent reduction in CCL19-mediated migration of Gab1-deficient mDCs to draining lymph nodes and subsequent impairment of Th2-driven adaptive activation. Mechanistically, Gab1 is an essential component of the CCL19/CCR7 chemokine axis that regulates mDC migration during asthmatic responses. Together, these findings provide the first evidence for the roles of Gab1 in lung, giving us deeper understanding of asthmatic pathogenesis.

Indexed as

Acute DiseaseAdaptor Proteins, Signal TransducingAnimalsAsthmaBronchoalveolar Lavage FluidCD11c AntigenCD4-Positive T-LymphocytesCell MovementChemokine CCL19Dendritic CellsDisease Models, AnimalHumansInterleukinsLeukocytes, MononuclearLungMiceAdaptor Proteins, Signal TransducingCD11c AntigenChemokine CCL19Gab1 protein, mouseInterleukinsPhosphoproteins

Identifiers

PMID27811945
PMCPMC5099873
OpenAlexW2548031726

What OpenQuestion holds

Textmetadata
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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.