PittsburghV1, PubMed, Checkpoint, bibRecord, 000509

Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.

Identifieur interne : 000509 ( PubMed/Checkpoint ); précédent : 000508; suivant : 000510

Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.

Auteurs : Chandrashekhar R. Gandhi [États-Unis] ; J Richard Chaillet [États-Unis] ; Michael A. Nalesnik [États-Unis] ; Sudhir Kumar [États-Unis] ; Anil Dangi [États-Unis] ; A Jake Demetris [États-Unis] ; Robert Ferrell [États-Unis] ; Tong Wu [États-Unis] ; Senad Divanovic [États-Unis] ; Traci Stankeiwicz [États-Unis] ; Benjamin Shaffer [États-Unis] ; Donna B. Stolz [États-Unis] ; Stephen A K. Harvey [États-Unis] ; Jiang Wang [États-Unis] ; Thomas E. Starzl [États-Unis]

Source :

Gastroenterology [ 1528-0012 ] ; 2015.

RBID : pubmed:25448926

Descripteurs français

KwdFr :
- Animaux, Apoptose, Carcinome hépatocellulaire (étiologie), Cirrhose expérimentale (étiologie), Cytochrome reductases (physiologie), Humains, Mitochondries (physiologie), Métabolisme des lipides, Oxidoreductases acting on sulfur group donors (physiologie), Régénération hépatique (physiologie), Souris, Souris knockout, Stéatose hépatique (étiologie), Tumeurs du foie (étiologie).
MESH :
- physiologie : Cytochrome reductases, Mitochondries, Oxidoreductases acting on sulfur group donors, Régénération hépatique.
- étiologie : Carcinome hépatocellulaire, Cirrhose expérimentale, Stéatose hépatique, Tumeurs du foie.
- Animaux, Apoptose, Humains, Métabolisme des lipides, Souris, Souris knockout.

English descriptors

KwdEn :
- Animals, Apoptosis, Carcinoma, Hepatocellular (etiology), Cytochrome Reductases (physiology), Fatty Liver (etiology), Humans, Lipid Metabolism, Liver Cirrhosis, Experimental (etiology), Liver Neoplasms (etiology), Liver Regeneration (physiology), Mice, Mice, Knockout, Mitochondria (physiology), Oxidoreductases Acting on Sulfur Group Donors (physiology).
MESH :
- chemical , physiology : Cytochrome Reductases, Oxidoreductases Acting on Sulfur Group Donors.
- etiology : Carcinoma, Hepatocellular, Fatty Liver, Liver Cirrhosis, Experimental, Liver Neoplasms.
- physiology : Liver Regeneration, Mitochondria.
- Animals, Apoptosis, Humans, Lipid Metabolism, Mice, Mice, Knockout.

Abstract

Augmenter of liver regeneration (ALR, encoded by GFER) is a widely distributed pleiotropic protein originally identified as a hepatic growth factor. However, little is known about its roles in hepatic physiology and pathology. We created mice with liver-specific deletion of ALR to study its function.

DOI: 10.1053/j.gastro.2014.10.008
PubMed: 25448926

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
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<author><name sortKey="Divanovic, Senad" sort="Divanovic, Senad" uniqKey="Divanovic S" first="Senad" last="Divanovic">Senad Divanovic</name>
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<wicri:cityArea>Department of Cell Biology, University of Pittsburgh</wicri:cityArea>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.</title>
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<author><name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Louisiane</region>
</placeName>
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<author><name sortKey="Stankeiwicz, Traci" sort="Stankeiwicz, Traci" uniqKey="Stankeiwicz T" first="Traci" last="Stankeiwicz">Traci Stankeiwicz</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Pennsylvanie</region>
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<placeName><region type="state">Ohio</region>
</placeName>
<wicri:cityArea>Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati</wicri:cityArea>
</affiliation>
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<term>Apoptosis</term>
<term>Carcinoma, Hepatocellular (etiology)</term>
<term>Cytochrome Reductases (physiology)</term>
<term>Fatty Liver (etiology)</term>
<term>Humans</term>
<term>Lipid Metabolism</term>
<term>Liver Cirrhosis, Experimental (etiology)</term>
<term>Liver Neoplasms (etiology)</term>
<term>Liver Regeneration (physiology)</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Mitochondria (physiology)</term>
<term>Oxidoreductases Acting on Sulfur Group Donors (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Carcinome hépatocellulaire (étiologie)</term>
<term>Cirrhose expérimentale (étiologie)</term>
<term>Cytochrome reductases (physiologie)</term>
<term>Humains</term>
<term>Mitochondries (physiologie)</term>
<term>Métabolisme des lipides</term>
<term>Oxidoreductases acting on sulfur group donors (physiologie)</term>
<term>Régénération hépatique (physiologie)</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Stéatose hépatique (étiologie)</term>
<term>Tumeurs du foie (étiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Cytochrome Reductases</term>
<term>Oxidoreductases Acting on Sulfur Group Donors</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Fatty Liver</term>
<term>Liver Cirrhosis, Experimental</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cytochrome reductases</term>
<term>Mitochondries</term>
<term>Oxidoreductases acting on sulfur group donors</term>
<term>Régénération hépatique</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Liver Regeneration</term>
<term>Mitochondria</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Cirrhose expérimentale</term>
<term>Stéatose hépatique</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Apoptosis</term>
<term>Humans</term>
<term>Lipid Metabolism</term>
<term>Mice</term>
<term>Mice, Knockout</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Humains</term>
<term>Métabolisme des lipides</term>
<term>Souris</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">Augmenter of liver regeneration (ALR, encoded by GFER) is a widely distributed pleiotropic protein originally identified as a hepatic growth factor. However, little is known about its roles in hepatic physiology and pathology. We created mice with liver-specific deletion of ALR to study its function.</div>
</front>
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<Day>24</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>02</Month>
<Day>20</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1528-0012</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>148</Volume>
<Issue>2</Issue>
<PubDate><Year>2015</Year>
<Month>Feb</Month>
</PubDate>
</JournalIssue>
<Title>Gastroenterology</Title>
<ISOAbbreviation>Gastroenterology</ISOAbbreviation>
</Journal>
<ArticleTitle>Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.</ArticleTitle>
<Pagination><MedlinePgn>379-391.e4</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1053/j.gastro.2014.10.008</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0016-5085(14)01207-4</ELocationID>
<Abstract><AbstractText Label="BACKGROUND & AIMS" NlmCategory="OBJECTIVE">Augmenter of liver regeneration (ALR, encoded by GFER) is a widely distributed pleiotropic protein originally identified as a hepatic growth factor. However, little is known about its roles in hepatic physiology and pathology. We created mice with liver-specific deletion of ALR to study its function.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">We developed mice with liver-specific deletion of ALR (ALR-L-KO) using the albumin-Cre/LoxP system. Liver tissues were collected from ALR-L-KO mice and ALR(floxed/floxed) mice (controls) and analyzed by histology, reverse-transcription polymerase chain reaction, immunohistochemistry, electron microscopy, and techniques to measure fibrosis and lipids. Liver tissues from patients with and without advanced liver disease were determined by immunoblot analysis.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Two weeks after birth, livers of ALR-L-KO mice contained low levels of ALR and adenosine triphosphate (ATP); they had reduced mitochondrial respiratory function and increased oxidative stress, compared with livers from control mice, and had excessive steatosis, and hepatocyte apoptosis. Levels of carbamyl-palmitoyl transferase 1a and ATP synthase subunit ATP5G1 were reduced in livers of ALR-L-KO mice, indicating defects in mitochondrial fatty acid transport and ATP synthesis. Electron microscopy showed mitochondrial swelling with abnormalities in shapes and numbers of cristae. From weeks 2-4 after birth, levels of steatosis and apoptosis decreased in ALR-L-KO mice, and numbers of ALR-expressing cells increased, along with ATP levels. However, at weeks 4-8 after birth, livers became inflamed, with hepatocellular necrosis, ductular proliferation, and fibrosis; hepatocellular carcinoma developed by 1 year after birth in nearly 60% of the mice. Hepatic levels of ALR were also low in ob/ob mice and alcohol-fed mice with liver steatosis, compared with controls. Levels of ALR were lower in liver tissues from patients with advanced alcoholic liver disease and nonalcoholic steatohepatitis than in control liver tissues.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">We developed mice with liver-specific deletion of ALR, and showed that it is required for mitochondrial function and lipid homeostasis in the liver. ALR-L-KO mice provide a useful model for investigating the pathogenesis of steatohepatitis and its complications.</AbstractText>
<CopyrightInformation>Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gandhi</LastName>
<ForeName>Chandrashekhar R</ForeName>
<Initials>CR</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Surgery, University of Cincinnati, Cincinnati, Ohio; Cincinnati VA Medical Center, Cincinnati, Ohio; Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh, Pennsylvania. Electronic address: gandhicr@ucmail.uc.edu.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chaillet</LastName>
<ForeName>J Richard</ForeName>
<Initials>JR</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nalesnik</LastName>
<ForeName>Michael A</ForeName>
<Initials>MA</Initials>
<AffiliationInfo><Affiliation>Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh, Pennsylvania; Department of Pathology, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kumar</LastName>
<ForeName>Sudhir</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dangi</LastName>
<ForeName>Anil</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Cincinnati, Cincinnati, Ohio; Cincinnati VA Medical Center, Cincinnati, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Demetris</LastName>
<ForeName>A Jake</ForeName>
<Initials>AJ</Initials>
<AffiliationInfo><Affiliation>Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh, Pennsylvania; Department of Pathology, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ferrell</LastName>
<ForeName>Robert</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>School of Public Health, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Tong</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, Louisiana.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Divanovic</LastName>
<ForeName>Senad</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Stankeiwicz</LastName>
<ForeName>Traci</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shaffer</LastName>
<ForeName>Benjamin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Stolz</LastName>
<ForeName>Donna B</ForeName>
<Initials>DB</Initials>
<AffiliationInfo><Affiliation>Department of Cell Biology, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Harvey</LastName>
<ForeName>Stephen A K</ForeName>
<Initials>SA</Initials>
<AffiliationInfo><Affiliation>Department of Ophthalmology, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jiang</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Starzl</LastName>
<ForeName>Thomas E</ForeName>
<Initials>TE</Initials>
<AffiliationInfo><Affiliation>Thomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>UL1 TR000005</GrantID>
<Acronym>TR</Acronym>
<Agency>NCATS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P01 AI081678</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 DK078392</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 DK054411</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R21 AA020846</GrantID>
<Acronym>AA</Acronym>
<Agency>NIAAA NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>I01 BX001174</GrantID>
<Acronym>BX</Acronym>
<Agency>BLRD VA</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>10</Month>
<Day>13</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Gastroenterology</MedlineTA>
<NlmUniqueID>0374630</NlmUniqueID>
<ISSNLinking>0016-5085</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>EC 1.6.2.-</RegistryNumber>
<NameOfSubstance UI="D003579">Cytochrome Reductases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.6.2.-</RegistryNumber>
<NameOfSubstance UI="C500897">GFER protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.8.-</RegistryNumber>
<NameOfSubstance UI="D050862">Oxidoreductases Acting on Sulfur Group Donors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.8.3.-</RegistryNumber>
<NameOfSubstance UI="C551231">GFER protein, mouse</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006528" MajorTopicYN="N">Carcinoma, Hepatocellular</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003579" MajorTopicYN="N">Cytochrome Reductases</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005234" MajorTopicYN="N">Fatty Liver</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050356" MajorTopicYN="N">Lipid Metabolism</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008106" MajorTopicYN="N">Liver Cirrhosis, Experimental</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008113" MajorTopicYN="N">Liver Neoplasms</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008115" MajorTopicYN="N">Liver Regeneration</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050862" MajorTopicYN="N">Oxidoreductases Acting on Sulfur Group Donors</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">NIHMS635133</OtherID>
<OtherID Source="NLM">PMC4802363</OtherID>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ALD</Keyword>
<Keyword MajorTopicYN="N">Augmenter of Liver Regeneration</Keyword>
<Keyword MajorTopicYN="N">Mouse Model</Keyword>
<Keyword MajorTopicYN="N">NASH</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year>
<Month>05</Month>
<Day>21</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2014</Year>
<Month>10</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2014</Year>
<Month>10</Month>
<Day>07</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2014</Year>
<Month>12</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2014</Year>
<Month>12</Month>
<Day>3</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>3</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25448926</ArticleId>
<ArticleId IdType="pii">S0016-5085(14)01207-4</ArticleId>
<ArticleId IdType="doi">10.1053/j.gastro.2014.10.008</ArticleId>
<ArticleId IdType="pmc">PMC4802363</ArticleId>
<ArticleId IdType="mid">NIHMS635133</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Louisiane</li>
<li>Ohio</li>
<li>Pennsylvanie</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Gandhi, Chandrashekhar R" sort="Gandhi, Chandrashekhar R" uniqKey="Gandhi C" first="Chandrashekhar R" last="Gandhi">Chandrashekhar R. Gandhi</name>
</region>
<name sortKey="Chaillet, J Richard" sort="Chaillet, J Richard" uniqKey="Chaillet J" first="J Richard" last="Chaillet">J Richard Chaillet</name>
<name sortKey="Dangi, Anil" sort="Dangi, Anil" uniqKey="Dangi A" first="Anil" last="Dangi">Anil Dangi</name>
<name sortKey="Demetris, A Jake" sort="Demetris, A Jake" uniqKey="Demetris A" first="A Jake" last="Demetris">A Jake Demetris</name>
<name sortKey="Divanovic, Senad" sort="Divanovic, Senad" uniqKey="Divanovic S" first="Senad" last="Divanovic">Senad Divanovic</name>
<name sortKey="Ferrell, Robert" sort="Ferrell, Robert" uniqKey="Ferrell R" first="Robert" last="Ferrell">Robert Ferrell</name>
<name sortKey="Harvey, Stephen A K" sort="Harvey, Stephen A K" uniqKey="Harvey S" first="Stephen A K" last="Harvey">Stephen A K. Harvey</name>
<name sortKey="Kumar, Sudhir" sort="Kumar, Sudhir" uniqKey="Kumar S" first="Sudhir" last="Kumar">Sudhir Kumar</name>
<name sortKey="Nalesnik, Michael A" sort="Nalesnik, Michael A" uniqKey="Nalesnik M" first="Michael A" last="Nalesnik">Michael A. Nalesnik</name>
<name sortKey="Shaffer, Benjamin" sort="Shaffer, Benjamin" uniqKey="Shaffer B" first="Benjamin" last="Shaffer">Benjamin Shaffer</name>
<name sortKey="Stankeiwicz, Traci" sort="Stankeiwicz, Traci" uniqKey="Stankeiwicz T" first="Traci" last="Stankeiwicz">Traci Stankeiwicz</name>
<name sortKey="Starzl, Thomas E" sort="Starzl, Thomas E" uniqKey="Starzl T" first="Thomas E" last="Starzl">Thomas E. Starzl</name>
<name sortKey="Stolz, Donna B" sort="Stolz, Donna B" uniqKey="Stolz D" first="Donna B" last="Stolz">Donna B. Stolz</name>
<name sortKey="Wang, Jiang" sort="Wang, Jiang" uniqKey="Wang J" first="Jiang" last="Wang">Jiang Wang</name>
<name sortKey="Wu, Tong" sort="Wu, Tong" uniqKey="Wu T" first="Tong" last="Wu">Tong Wu</name>
</country>
</tree>
</affiliations>
</record>

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       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a PittsburghV1

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Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.

Liver-specific deletion of augmenter of liver regeneration accelerates development of steatohepatitis and hepatocellular carcinoma in mice.

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