RapamycinFungusV1, Main, Exploration, bibRecord, 000333

High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.

Identifieur interne : 000333 ( Main/Exploration ); précédent : 000332; suivant : 000334

High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.

Source :

Biochemical and biophysical research communications [ 1090-2104 ] ; 2019.

RBID : pubmed:30952427

Descripteurs français

English descriptors

KwdEn :
- AMP-Activated Protein Kinases (metabolism), Animals (MeSH), Autophagy (MeSH), Autophagy-Related Protein-1 Homolog (metabolism), Cell Line (MeSH), Cell Proliferation (MeSH), Epithelial Cells (cytology), Epithelial Cells (metabolism), Epithelial Cells (microbiology), Escherichia coli (growth & development), Escherichia coli (metabolism), Escherichia coli Infections (metabolism), Escherichia coli Infections (microbiology), Female (MeSH), HMGN2 Protein (metabolism), Humans (MeSH), Mice, Inbred C57BL (MeSH), Signal Transduction (MeSH), Urinary Bladder (cytology), Urinary Bladder (metabolism), Urinary Bladder (microbiology), Urinary Tract Infections (metabolism), Urinary Tract Infections (microbiology).
MESH :
- chemical , metabolism : AMP-Activated Protein Kinases, Autophagy-Related Protein-1 Homolog, HMGN2 Protein.
- cytology : Epithelial Cells, Urinary Bladder.
- growth & development : Escherichia coli.
- metabolism : Epithelial Cells, Escherichia coli, Escherichia coli Infections, Urinary Bladder, Urinary Tract Infections.
- microbiology : Epithelial Cells, Escherichia coli Infections, Urinary Bladder, Urinary Tract Infections.
- Animals, Autophagy, Cell Line, Cell Proliferation, Female, Humans, Mice, Inbred C57BL, Signal Transduction.

Abstract

Urinary tract infection is one of the most common bacterial infections which is mainly caused by Escherichia coli (UPEC). Autophagy plays a key role in immune response to eliminate invading pathogens. Exploring the effect of autophagy on UPEC infection and the molecular mechanisms will be benefit for the treatment of urinary tract infection. High-mobility group protein N2 (HMGN2), a highly conserved nuclear protein and an antibacterial peptide, has been associated with bacterial infection induced immune response; however, whether this function is due to the regulation of autophagy remains unclear. In this study, we demonstrate for the first time that HMGN2 is upregulated in UPEC infection of bladder epithelial cell line 5637 (BEC 5637). Furthermore, HMGN2 enhances autophagy in BEC 5637 via activation of AMPK and ULK1, whereas UPEC suppresses autophagy. In addition, the enhanced autophagy activity by HMGN2 overexpression or rapamycin boosts the proliferation of UPEC J96 in BEC 5637. In summary, our data indicate that HMGN2 activates autophagy via AMPK/ULK1 pathway which can be utilized by UPEC J96 for their proliferation within bladder epithelial cells.

DOI: 10.1016/j.bbrc.2019.03.062
PubMed: 30952427

Affiliations:

République populaire de Chine

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Le document en format XML

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<author><name sortKey="Ren, Laibin" sort="Ren, Laibin" uniqKey="Ren L" first="Laibin" last="Ren">Laibin Ren</name>
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<author><name sortKey="Lu, Kefeng" sort="Lu, Kefeng" uniqKey="Lu K" first="Kefeng" last="Lu">Kefeng Lu</name>
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<author><name sortKey="Li, Dongze" sort="Li, Dongze" uniqKey="Li D" first="Dongze" last="Li">Dongze Li</name>
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<author><name sortKey="Zeng, Rui" sort="Zeng, Rui" uniqKey="Zeng R" first="Rui" last="Zeng">Rui Zeng</name>
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<author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name>
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<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
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<author><name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name>
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<author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.</title>
<author><name sortKey="Zhang, Fumei" sort="Zhang, Fumei" uniqKey="Zhang F" first="Fumei" last="Zhang">Fumei Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China; Experimental Center, Northwest Minzu University, Lanzhou, Gansu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China; Experimental Center, Northwest Minzu University, Lanzhou, Gansu</wicri:regionArea>
<wicri:noRegion>Gansu</wicri:noRegion>
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<author><name sortKey="Zhu, Feimei" sort="Zhu, Feimei" uniqKey="Zhu F" first="Feimei" last="Zhu">Feimei Zhu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yang, Jinhao" sort="Yang, Jinhao" uniqKey="Yang J" first="Jinhao" last="Yang">Jinhao Yang</name>
<affiliation wicri:level="1"><nlm:affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
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<author><name sortKey="Zhang, Wen" sort="Zhang, Wen" uniqKey="Zhang W" first="Wen" last="Zhang">Wen Zhang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>West China Medical School, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
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<author><name sortKey="Liu, Keyun" sort="Liu, Keyun" uniqKey="Liu K" first="Keyun" last="Liu">Keyun Liu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Physiology, School of Medicine, Hubei University for Nationalities, Enshi, Hubei</wicri:regionArea>
<wicri:noRegion>Hubei</wicri:noRegion>
</affiliation>
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<author><name sortKey="Ren, Laibin" sort="Ren, Laibin" uniqKey="Ren L" first="Laibin" last="Ren">Laibin Ren</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Xiong, Feng" sort="Xiong, Feng" uniqKey="Xiong F" first="Feng" last="Xiong">Feng Xiong</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lu, Kefeng" sort="Lu, Kefeng" uniqKey="Lu K" first="Kefeng" last="Lu">Kefeng Lu</name>
<affiliation wicri:level="1"><nlm:affiliation>State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu</wicri:regionArea>
<wicri:noRegion>Chengdu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Dongze" sort="Li, Dongze" uniqKey="Li D" first="Dongze" last="Li">Dongze Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu</wicri:regionArea>
<wicri:noRegion>Chengdu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zeng, Rui" sort="Zeng, Rui" uniqKey="Zeng R" first="Rui" last="Zeng">Rui Zeng</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Cardiology, West China Hospital, Sichuan University, Chengdu</wicri:regionArea>
<wicri:noRegion>Chengdu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
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<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
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<author><name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China. Electronic address: chenjunlinsf@163.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China. Electronic address: ninghuangcjl@163.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan</wicri:regionArea>
<wicri:noRegion>Sichuan</wicri:noRegion>
</affiliation>
</author>
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<series><title level="j">Biochemical and biophysical research communications</title>
<idno type="eISSN">1090-2104</idno>
<imprint><date when="2019" type="published">2019</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Autophagy (MeSH)</term>
<term>Autophagy-Related Protein-1 Homolog (metabolism)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Epithelial Cells (cytology)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Epithelial Cells (microbiology)</term>
<term>Escherichia coli (growth & development)</term>
<term>Escherichia coli (metabolism)</term>
<term>Escherichia coli Infections (metabolism)</term>
<term>Escherichia coli Infections (microbiology)</term>
<term>Female (MeSH)</term>
<term>HMGN2 Protein (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Urinary Bladder (cytology)</term>
<term>Urinary Bladder (metabolism)</term>
<term>Urinary Bladder (microbiology)</term>
<term>Urinary Tract Infections (metabolism)</term>
<term>Urinary Tract Infections (microbiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>AMP-Activated Protein Kinases (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Autophagie (MeSH)</term>
<term>Cellules épithéliales (cytologie)</term>
<term>Cellules épithéliales (microbiologie)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Escherichia coli (croissance et développement)</term>
<term>Escherichia coli (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Homologue de la protéine-1 associée à l'autophagie (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Infections urinaires (microbiologie)</term>
<term>Infections urinaires (métabolisme)</term>
<term>Infections à Escherichia coli (microbiologie)</term>
<term>Infections à Escherichia coli (métabolisme)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéine HMGN2 (métabolisme)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Vessie urinaire (cytologie)</term>
<term>Vessie urinaire (microbiologie)</term>
<term>Vessie urinaire (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>AMP-Activated Protein Kinases</term>
<term>Autophagy-Related Protein-1 Homolog</term>
<term>HMGN2 Protein</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Escherichia coli</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Vessie urinaire</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Epithelial Cells</term>
<term>Urinary Bladder</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Escherichia coli</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
<term>Escherichia coli</term>
<term>Escherichia coli Infections</term>
<term>Urinary Bladder</term>
<term>Urinary Tract Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Infections urinaires</term>
<term>Infections à Escherichia coli</term>
<term>Vessie urinaire</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Epithelial Cells</term>
<term>Escherichia coli Infections</term>
<term>Urinary Bladder</term>
<term>Urinary Tract Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Cellules épithéliales</term>
<term>Escherichia coli</term>
<term>Homologue de la protéine-1 associée à l'autophagie</term>
<term>Infections urinaires</term>
<term>Infections à Escherichia coli</term>
<term>Protéine HMGN2</term>
<term>Vessie urinaire</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Autophagy</term>
<term>Cell Line</term>
<term>Cell Proliferation</term>
<term>Female</term>
<term>Humans</term>
<term>Mice, Inbred C57BL</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Autophagie</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Prolifération cellulaire</term>
<term>Souris de lignée C57BL</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Urinary tract infection is one of the most common bacterial infections which is mainly caused by Escherichia coli (UPEC). Autophagy plays a key role in immune response to eliminate invading pathogens. Exploring the effect of autophagy on UPEC infection and the molecular mechanisms will be benefit for the treatment of urinary tract infection. High-mobility group protein N2 (HMGN2), a highly conserved nuclear protein and an antibacterial peptide, has been associated with bacterial infection induced immune response; however, whether this function is due to the regulation of autophagy remains unclear. In this study, we demonstrate for the first time that HMGN2 is upregulated in UPEC infection of bladder epithelial cell line 5637 (BEC 5637). Furthermore, HMGN2 enhances autophagy in BEC 5637 via activation of AMPK and ULK1, whereas UPEC suppresses autophagy. In addition, the enhanced autophagy activity by HMGN2 overexpression or rapamycin boosts the proliferation of UPEC J96 in BEC 5637. In summary, our data indicate that HMGN2 activates autophagy via AMPK/ULK1 pathway which can be utilized by UPEC J96 for their proliferation within bladder epithelial cells.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30952427</PMID>
<DateCompleted><Year>2020</Year>
<Month>04</Month>
<Day>06</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>04</Month>
<Day>08</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>513</Volume>
<Issue>1</Issue>
<PubDate><Year>2019</Year>
<Month>05</Month>
<Day>21</Day>
</PubDate>
</JournalIssue>
<Title>Biochemical and biophysical research communications</Title>
<ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation>
</Journal>
<ArticleTitle>High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.</ArticleTitle>
<Pagination><MedlinePgn>193-200</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0006-291X(19)30439-5</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2019.03.062</ELocationID>
<Abstract><AbstractText>Urinary tract infection is one of the most common bacterial infections which is mainly caused by Escherichia coli (UPEC). Autophagy plays a key role in immune response to eliminate invading pathogens. Exploring the effect of autophagy on UPEC infection and the molecular mechanisms will be benefit for the treatment of urinary tract infection. High-mobility group protein N2 (HMGN2), a highly conserved nuclear protein and an antibacterial peptide, has been associated with bacterial infection induced immune response; however, whether this function is due to the regulation of autophagy remains unclear. In this study, we demonstrate for the first time that HMGN2 is upregulated in UPEC infection of bladder epithelial cell line 5637 (BEC 5637). Furthermore, HMGN2 enhances autophagy in BEC 5637 via activation of AMPK and ULK1, whereas UPEC suppresses autophagy. In addition, the enhanced autophagy activity by HMGN2 overexpression or rapamycin boosts the proliferation of UPEC J96 in BEC 5637. In summary, our data indicate that HMGN2 activates autophagy via AMPK/ULK1 pathway which can be utilized by UPEC J96 for their proliferation within bladder epithelial cells.</AbstractText>
<CopyrightInformation>Copyright © 2019. Published by Elsevier Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Fumei</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China; Experimental Center, Northwest Minzu University, Lanzhou, Gansu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Feimei</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Jinhao</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Wen</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Keyun</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Physiology, School of Medicine, Hubei University for Nationalities, Enshi, Hubei, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ren</LastName>
<ForeName>Laibin</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xiong</LastName>
<ForeName>Feng</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lu</LastName>
<ForeName>Kefeng</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Dongze</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zeng</LastName>
<ForeName>Rui</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xiaoying</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jingyu</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Shanze</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Junli</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China. Electronic address: chenjunlinsf@163.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Ning</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China. Electronic address: ninghuangcjl@163.com.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>04</Month>
<Day>02</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Biochem Biophys Res Commun</MedlineTA>
<NlmUniqueID>0372516</NlmUniqueID>
<ISSNLinking>0006-291X</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D024242">HMGN2 Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000071189">Autophagy-Related Protein-1 Homolog</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber>
<NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071189" MajorTopicYN="N">Autophagy-Related Protein-1 Homolog</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004926" MajorTopicYN="N">Escherichia coli</DescriptorName>
<QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004927" MajorTopicYN="N">Escherichia coli Infections</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D024242" MajorTopicYN="N">HMGN2 Protein</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001743" MajorTopicYN="N">Urinary Bladder</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014552" MajorTopicYN="N">Urinary Tract Infections</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">AMPK</Keyword>
<Keyword MajorTopicYN="Y">Autophagy</Keyword>
<Keyword MajorTopicYN="Y">HMGN2</Keyword>
<Keyword MajorTopicYN="Y">ULK1</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
<Month>02</Month>
<Day>18</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>03</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2019</Year>
<Month>4</Month>
<Day>7</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>4</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2019</Year>
<Month>4</Month>
<Day>7</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">30952427</ArticleId>
<ArticleId IdType="pii">S0006-291X(19)30439-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.bbrc.2019.03.062</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Fumei" sort="Zhang, Fumei" uniqKey="Zhang F" first="Fumei" last="Zhang">Fumei Zhang</name>
</noRegion>
<name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name>
<name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name>
<name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name>
<name sortKey="Li, Dongze" sort="Li, Dongze" uniqKey="Li D" first="Dongze" last="Li">Dongze Li</name>
<name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name>
<name sortKey="Liu, Keyun" sort="Liu, Keyun" uniqKey="Liu K" first="Keyun" last="Liu">Keyun Liu</name>
<name sortKey="Lu, Kefeng" sort="Lu, Kefeng" uniqKey="Lu K" first="Kefeng" last="Lu">Kefeng Lu</name>
<name sortKey="Ren, Laibin" sort="Ren, Laibin" uniqKey="Ren L" first="Laibin" last="Ren">Laibin Ren</name>
<name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name>
<name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<name sortKey="Xiong, Feng" sort="Xiong, Feng" uniqKey="Xiong F" first="Feng" last="Xiong">Feng Xiong</name>
<name sortKey="Yang, Jinhao" sort="Yang, Jinhao" uniqKey="Yang J" first="Jinhao" last="Yang">Jinhao Yang</name>
<name sortKey="Zeng, Rui" sort="Zeng, Rui" uniqKey="Zeng R" first="Rui" last="Zeng">Rui Zeng</name>
<name sortKey="Zhang, Wen" sort="Zhang, Wen" uniqKey="Zhang W" first="Wen" last="Zhang">Wen Zhang</name>
<name sortKey="Zhu, Feimei" sort="Zhu, Feimei" uniqKey="Zhu F" first="Feimei" last="Zhu">Feimei Zhu</name>
</country>
</tree>
</affiliations>
</record>

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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.

High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.

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