High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.
Identifieur interne : 000307 ( Main/Corpus ); précédent : 000306; suivant : 000308High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.
Auteurs : Fumei Zhang ; Feimei Zhu ; Jinhao Yang ; Wen Zhang ; Keyun Liu ; Laibin Ren ; Feng Xiong ; Kefeng Lu ; Dongze Li ; Rui Zeng ; Xiaoying Wang ; Jingyu Li ; Shanze Chen ; Yi Wang ; Junli Chen ; Ning HuangSource :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2019.
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
Links to Exploration step
pubmed:30952427Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><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><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></affiliation></author><author><name sortKey="Zhu, Feimei" sort="Zhu, Feimei" uniqKey="Zhu F" first="Feimei" last="Zhu">Feimei Zhu</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jinhao" sort="Yang, Jinhao" uniqKey="Yang J" first="Jinhao" last="Yang">Jinhao Yang</name><affiliation><nlm:affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Wen" sort="Zhang, Wen" uniqKey="Zhang W" first="Wen" last="Zhang">Wen Zhang</name><affiliation><nlm:affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Keyun" sort="Liu, Keyun" uniqKey="Liu K" first="Keyun" last="Liu">Keyun Liu</name><affiliation><nlm:affiliation>Department of Physiology, School of Medicine, Hubei University for Nationalities, Enshi, Hubei, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ren, Laibin" sort="Ren, Laibin" uniqKey="Ren L" first="Laibin" last="Ren">Laibin Ren</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xiong, Feng" sort="Xiong, Feng" uniqKey="Xiong F" first="Feng" last="Xiong">Feng Xiong</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, Kefeng" sort="Lu, Kefeng" uniqKey="Lu K" first="Kefeng" last="Lu">Kefeng Lu</name><affiliation><nlm:affiliation>State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Dongze" sort="Li, Dongze" uniqKey="Li D" first="Dongze" last="Li">Dongze Li</name><affiliation><nlm:affiliation>Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zeng, Rui" sort="Zeng, Rui" uniqKey="Zeng R" first="Rui" last="Zeng">Rui Zeng</name><affiliation><nlm:affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name><affiliation><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></affiliation></author><author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name><affiliation><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></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:30952427</idno><idno type="pmid">30952427</idno><idno type="doi">10.1016/j.bbrc.2019.03.062</idno><idno type="wicri:Area/Main/Corpus">000307</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000307</idno></publicationStmt><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><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></affiliation></author><author><name sortKey="Zhu, Feimei" sort="Zhu, Feimei" uniqKey="Zhu F" first="Feimei" last="Zhu">Feimei Zhu</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jinhao" sort="Yang, Jinhao" uniqKey="Yang J" first="Jinhao" last="Yang">Jinhao Yang</name><affiliation><nlm:affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Wen" sort="Zhang, Wen" uniqKey="Zhang W" first="Wen" last="Zhang">Wen Zhang</name><affiliation><nlm:affiliation>West China Medical School, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Keyun" sort="Liu, Keyun" uniqKey="Liu K" first="Keyun" last="Liu">Keyun Liu</name><affiliation><nlm:affiliation>Department of Physiology, School of Medicine, Hubei University for Nationalities, Enshi, Hubei, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ren, Laibin" sort="Ren, Laibin" uniqKey="Ren L" first="Laibin" last="Ren">Laibin Ren</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xiong, Feng" sort="Xiong, Feng" uniqKey="Xiong F" first="Feng" last="Xiong">Feng Xiong</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Lu, Kefeng" sort="Lu, Kefeng" uniqKey="Lu K" first="Kefeng" last="Lu">Kefeng Lu</name><affiliation><nlm:affiliation>State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Dongze" sort="Li, Dongze" uniqKey="Li D" first="Dongze" last="Li">Dongze Li</name><affiliation><nlm:affiliation>Department of Emergency Medicine, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zeng, Rui" sort="Zeng, Rui" uniqKey="Zeng R" first="Rui" last="Zeng">Rui Zeng</name><affiliation><nlm:affiliation>Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Xiaoying" sort="Wang, Xiaoying" uniqKey="Wang X" first="Xiaoying" last="Wang">Xiaoying Wang</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Jingyu" sort="Li, Jingyu" uniqKey="Li J" first="Jingyu" last="Li">Jingyu Li</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Shanze" sort="Chen, Shanze" uniqKey="Chen S" first="Shanze" last="Chen">Shanze Chen</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name><affiliation><nlm:affiliation>Department of Pathophysiology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Junli" sort="Chen, Junli" uniqKey="Chen J" first="Junli" last="Chen">Junli Chen</name><affiliation><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></affiliation></author><author><name sortKey="Huang, Ning" sort="Huang, Ning" uniqKey="Huang N" first="Ning" last="Huang">Ning Huang</name><affiliation><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></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><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="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="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="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" 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></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></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000307 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000307 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:30952427
|texte= High-mobility group protein N2 induces autophagy by activating AMPK/ULK1 pathway and thereby boosts UPEC proliferation within bladder epithelial cells.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:30952427" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |