Evidence map›Paper›PMID 32841502›Full record

ArticleJournal of cellular and molecular medicine2020

LKB1-MARK2 signalling mediates lipopolysaccharide-induced production of cytokines in mouse macrophages.

Jie Deng, Chunmei Wen, Xiangyu Ding, Xi Zhang, Guoqing Hou, Andong Liu, Hui Xu, Xuan Cao, Yongheng Bai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Jie DengKey Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Chunmei WenKey Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Xiangyu DingSchool of Ophthalmology and Optometry and Eye Hospital, Wenzhou Medical University, Wenzhou, China.
Xi ZhangDepartment of Medical Genetics, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Guoqing HouDepartment of Medical Genetics, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Andong LiuDepartment of Medical Genetics, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui XuUltrastructural Pathology Laboratory, Department of Pathology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xuan CaoDepartment of Medical Genetics, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yongheng BaiKey Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.ORCID 0000-0003-3910-4731
Huazhong University of Science and Technology · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipopolysaccharide (LPS) is an endotoxin involved in a number of acute and chronic inflammatory syndromes. Although LPS-induced signalling has been extensively studied, there are still mysteries remaining to be revealed. In the current study, we used high-throughput phosphoproteomics to profile LPS-initiated signalling and aimed to find novel mediators. A total of 448 phosphoproteins with 765 phosphorylation sites were identified, and we further validated that the phosphorylation of MARK2 on T208 was important for the regulation on LPS-induced CXCL15 (human IL-8 homolog), IL-1β, IL-6 and TNF-α release, in which LKB1 had a significant contribution. In summary, induction of cytokines by LPS in mouse macrophage is regulated by LKB1-MARK2 signals. Our study provides new clues for further exploring the underlying mechanisms of LPS-induced diseases, and new therapeutic approaches concerning bacterial infection may be derived from these findings.

Indexed as

Signal TransductionAMP-Activated Protein KinasesAnimalsCell Cycle ProteinsChemokines, CXCHeLa CellsHumansLipopolysaccharidesMacrophagesMiceModels, BiologicalPhosphoprotein PhosphatasesPhosphorylationProtein Serine-Threonine KinasesRAW 264.7 CellsTranscription FactorsAMP-Activated Protein KinasesCell Cycle ProteinsChemokines, CXCCxcl15 protein, mouseLipopolysaccharidesMark2 protein, mousePhosphoprotein PhosphatasesProtein Serine-Threonine KinasesStk11 protein, mouseTranscription FactorscytokinelipopolysaccharideLKB1MARK2phosphorylation

Identifiers

PMID32841502
PMCPMC7576310
OpenAlexW3080486908

What OpenQuestion holds

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LicenceCC BY
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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.