Evidence map›Paper›PMID 35766380›Full record

ArticlemBio2022

Interactions of Bacterial Toxin CNF1 and Host JAK1/2 Driven by Liquid-Liquid Phase Separation Enhance Macrophage Polarization.

Xuan Sun, Jianming Yang, Xueqin Deng, Yuting Wei, Changying Wang, Yaxiu Guo, Huan Yang, Liu Yang, Chunhui Miao, Junqiang Lv and 4 more

Open access · goldAbstract read
In one paragraph

Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 10 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

14 authors at 1 institution in 1 country.

Xuan Sun *Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Jianming Yang *Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Xueqin Deng *Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Yuting WeiKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Changying WangKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Yaxiu GuoKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Huan YangKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.ORCID 0000-0002-1511-6159
Liu YangKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Chunhui MiaoKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Junqiang LvKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Yawen XiaoKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Hong ZhangKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Zhi YaoKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.
Quan WangKey Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Institute of Urology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical Universitygrid.265021.2grid.412645.0, Tianjin, China.ORCID 0000-0003-4997-7173
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urinary tract infections (UTIs) are a global public health concern, which is mainly caused by uropathogenic Escherichia coli (UPEC). Cytotoxic necrotizing factor 1 (CNF1) is a key UPEC toxin and regulates multiple host cellular processes through activating the Rho GTPases; however, the effect of CNF1 on macrophage polarization remains unknown. Here, we found that CNF1 promoted M1 macrophage polarization through regulating NF-κB and JAK-STAT1 signaling pathways in kidney at an early stage of acute UTIs. Notably, we identified CNF1 could directly interact with JAK1/2 through its domain without Rho GTPases activation, which induced JAK1/2 phosphorylation, subsequent STAT1 activation and M1 polarization. Moreover, CNF1 exhibited liquid-liquid phase separation (LLPS) to induce a CNF1-JAK1/2 complex, promoting macrophage reprogramming. These findings highlight the LLPS-dependent and Rho GTPase-independent effect of CNF1 as an adaptor on interfering with host cell signals.

Indexed as

Bacterial ToxinsEscherichia coli ProteinsUrinary Tract InfectionsUropathogenic Escherichia coliHumansInflammationJanus Kinase 1Macrophagesrho GTP-Binding ProteinsBacterial Toxinscytotoxic necrotizing factor type 1Escherichia coli ProteinsJAK1 protein, humanJanus Kinase 1rho GTP-Binding ProteinsCNF1JAK-STAT1liquid-liquid phase separationmacrophage polarization

Identifiers

PMID35766380
PMCPMC9426534
OpenAlexW4283732685

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.