RapamycinFungusV1, Main, Exploration, bibRecord, 000688

mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.

Identifieur interne : 000688 ( Main/Exploration ); précédent : 000687; suivant : 000689

mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.

Auteurs : Kristin Dauner ; Walaa Eid [Canada] ; Riya Raghupathy ; John F. Presley [Canada] ; Xiaohui Zha [Canada]

Source :

The Journal of biological chemistry [ 1083-351X ] ; 2017.

RBID : pubmed:28196862

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Autophagy-Related Protein 5 (genetics), Autophagy-Related Protein 5 (metabolism), Biological Transport, Active (physiology), Cell Proliferation (physiology), Cells, Cultured (MeSH), Embryo, Mammalian (cytology), Embryo, Mammalian (metabolism), Endocytosis (physiology), Endosomal Sorting Complexes Required for Transport (genetics), Endosomal Sorting Complexes Required for Transport (metabolism), Fibroblasts (cytology), Fibroblasts (metabolism), Lysosomes (genetics), Lysosomes (metabolism), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Sphingomyelins (genetics), Sphingomyelins (metabolism), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Transferrin (genetics), Transferrin (metabolism).
MESH :
- chemical , genetics : Autophagy-Related Protein 5, Endosomal Sorting Complexes Required for Transport, Multiprotein Complexes, Sphingomyelins, TOR Serine-Threonine Kinases, Transferrin.
- chemical , metabolism : Autophagy-Related Protein 5, Endosomal Sorting Complexes Required for Transport, Multiprotein Complexes, Sphingomyelins, TOR Serine-Threonine Kinases, Transferrin.
- cytology : Embryo, Mammalian, Fibroblasts.
- genetics : Lysosomes.
- metabolism : Embryo, Mammalian, Fibroblasts, Lysosomes.
- physiology : Biological Transport, Active, Cell Proliferation, Endocytosis.
- Animals, Cells, Cultured, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Knockout.

Abstract

The plasma membrane of mammalian cells undergoes constitutive endocytosis, endocytic sorting, and recycling, which delivers nutrients to the lysosomes. The receptors, along with membrane lipids, are normally returned to the plasma membrane to sustain this action. It is not known, however, whether this process is influenced by metabolic conditions. Here we report that endocytic recycling requires active mechanistic target of rapamycin (aka mammalian target of rapamycin) (mTORC1), a master metabolic sensor. Upon mTORC1 inactivation, either by starvation or by inhibitor, recycling receptors and plasma membrane lipids, such as transferrin receptors and sphingomyelin, are delivered to the lysosomes. This lysosomal targeting is independent of canonical autophagy: both WT and Atg5^-/- mouse embryonic fibroblasts responded similarly. Furthermore, we identify hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs), an endosomal sorting complexes required for transport (ESCORT-0) component, as a downstream target of mTORC1. Hrs requires mTORC1 activity to maintain its protein expression level. Silencing Hrs without decreasing mTORC1 activity is sufficient to target transferrin and sphingomyelin to the lysosomes. It is thus evident that the canonical recycling pathway is under the regulation of mTORC1 and likely most predominant in proliferating cells where mTORC1 is highly active.

DOI: 10.1074/jbc.M116.771451
PubMed: 28196862
PubMed Central: PMC5392569

Affiliations:

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

to stream Main, to step Corpus: 000873
to stream Main, to step Curation: 000873

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.</title>
<author><name sortKey="Dauner, Kristin" sort="Dauner, Kristin" uniqKey="Dauner K" first="Kristin" last="Dauner">Kristin Dauner</name>
<affiliation><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</nlm:affiliation>
<wicri:noCountry code="subField">Ottawa Hospital Research Institute and</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Eid, Walaa" sort="Eid, Walaa" uniqKey="Eid W" first="Walaa" last="Eid">Walaa Eid</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6</wicri:regionArea>
<wicri:noRegion>Ontario K1H 8L6</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Raghupathy, Riya" sort="Raghupathy, Riya" uniqKey="Raghupathy R" first="Riya" last="Raghupathy">Riya Raghupathy</name>
<affiliation><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</nlm:affiliation>
<wicri:noCountry code="subField">Ottawa Hospital Research Institute and</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Presley, John F" sort="Presley, John F" uniqKey="Presley J" first="John F" last="Presley">John F. Presley</name>
<affiliation wicri:level="4"><nlm:affiliation>the Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>the Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7</wicri:regionArea>
<orgName type="university">Université McGill</orgName>
<placeName><settlement type="city">Montréal</settlement>
<region type="state">Québec</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zha, Xiaohui" sort="Zha, Xiaohui" uniqKey="Zha X" first="Xiaohui" last="Zha">Xiaohui Zha</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and xzha@ohri.ca.</nlm:affiliation>
<country wicri:rule="url">Canada</country>
<wicri:regionArea>From the Chronic Disease Program</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6</wicri:regionArea>
<wicri:noRegion>Ontario K1H 8L6</wicri:noRegion>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2017">2017</date>
<idno type="RBID">pubmed:28196862</idno>
<idno type="pmid">28196862</idno>
<idno type="doi">10.1074/jbc.M116.771451</idno>
<idno type="pmc">PMC5392569</idno>
<idno type="wicri:Area/Main/Corpus">000873</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000873</idno>
<idno type="wicri:Area/Main/Curation">000873</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000873</idno>
<idno type="wicri:Area/Main/Exploration">000873</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.</title>
<author><name sortKey="Dauner, Kristin" sort="Dauner, Kristin" uniqKey="Dauner K" first="Kristin" last="Dauner">Kristin Dauner</name>
<affiliation><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</nlm:affiliation>
<wicri:noCountry code="subField">Ottawa Hospital Research Institute and</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Eid, Walaa" sort="Eid, Walaa" uniqKey="Eid W" first="Walaa" last="Eid">Walaa Eid</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6</wicri:regionArea>
<wicri:noRegion>Ontario K1H 8L6</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Raghupathy, Riya" sort="Raghupathy, Riya" uniqKey="Raghupathy R" first="Riya" last="Raghupathy">Riya Raghupathy</name>
<affiliation><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</nlm:affiliation>
<wicri:noCountry code="subField">Ottawa Hospital Research Institute and</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Presley, John F" sort="Presley, John F" uniqKey="Presley J" first="John F" last="Presley">John F. Presley</name>
<affiliation wicri:level="4"><nlm:affiliation>the Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>the Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7</wicri:regionArea>
<orgName type="university">Université McGill</orgName>
<placeName><settlement type="city">Montréal</settlement>
<region type="state">Québec</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zha, Xiaohui" sort="Zha, Xiaohui" uniqKey="Zha X" first="Xiaohui" last="Zha">Xiaohui Zha</name>
<affiliation wicri:level="1"><nlm:affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and xzha@ohri.ca.</nlm:affiliation>
<country wicri:rule="url">Canada</country>
<wicri:regionArea>From the Chronic Disease Program</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6</wicri:regionArea>
<wicri:noRegion>Ontario K1H 8L6</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">The Journal of biological chemistry</title>
<idno type="eISSN">1083-351X</idno>
<imprint><date when="2017" type="published">2017</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Autophagy-Related Protein 5 (genetics)</term>
<term>Autophagy-Related Protein 5 (metabolism)</term>
<term>Biological Transport, Active (physiology)</term>
<term>Cell Proliferation (physiology)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Embryo, Mammalian (cytology)</term>
<term>Embryo, Mammalian (metabolism)</term>
<term>Endocytosis (physiology)</term>
<term>Endosomal Sorting Complexes Required for Transport (genetics)</term>
<term>Endosomal Sorting Complexes Required for Transport (metabolism)</term>
<term>Fibroblasts (cytology)</term>
<term>Fibroblasts (metabolism)</term>
<term>Lysosomes (genetics)</term>
<term>Lysosomes (metabolism)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Multiprotein Complexes (genetics)</term>
<term>Multiprotein Complexes (metabolism)</term>
<term>Sphingomyelins (genetics)</term>
<term>Sphingomyelins (metabolism)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Transferrin (genetics)</term>
<term>Transferrin (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term>
<term>Complexes de tri endosomique requis pour le transport (génétique)</term>
<term>Complexes de tri endosomique requis pour le transport (métabolisme)</term>
<term>Complexes multiprotéiques (génétique)</term>
<term>Complexes multiprotéiques (métabolisme)</term>
<term>Embryon de mammifère (cytologie)</term>
<term>Embryon de mammifère (métabolisme)</term>
<term>Endocytose (physiologie)</term>
<term>Fibroblastes (cytologie)</term>
<term>Fibroblastes (métabolisme)</term>
<term>Lysosomes (génétique)</term>
<term>Lysosomes (métabolisme)</term>
<term>Prolifération cellulaire (physiologie)</term>
<term>Protéine-5 associée à l'autophagie (génétique)</term>
<term>Protéine-5 associée à l'autophagie (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Sphingomyéline (génétique)</term>
<term>Sphingomyéline (métabolisme)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transferrine (génétique)</term>
<term>Transferrine (métabolisme)</term>
<term>Transport biologique actif (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>Endosomal Sorting Complexes Required for Transport</term>
<term>Multiprotein Complexes</term>
<term>Sphingomyelins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transferrin</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>Endosomal Sorting Complexes Required for Transport</term>
<term>Multiprotein Complexes</term>
<term>Sphingomyelins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transferrin</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Embryon de mammifère</term>
<term>Fibroblastes</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Embryo, Mammalian</term>
<term>Fibroblasts</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complexes de tri endosomique requis pour le transport</term>
<term>Complexes multiprotéiques</term>
<term>Lysosomes</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Sphingomyéline</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transferrine</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Embryo, Mammalian</term>
<term>Fibroblasts</term>
<term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complexes de tri endosomique requis pour le transport</term>
<term>Complexes multiprotéiques</term>
<term>Embryon de mammifère</term>
<term>Fibroblastes</term>
<term>Lysosomes</term>
<term>Protéine-5 associée à l'autophagie</term>
<term>Sphingomyéline</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transferrine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Endocytose</term>
<term>Prolifération cellulaire</term>
<term>Transport biologique actif</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Biological Transport, Active</term>
<term>Cell Proliferation</term>
<term>Endocytosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cells, Cultured</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Mice</term>
<term>Mice, Knockout</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Souris</term>
<term>Souris knockout</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The plasma membrane of mammalian cells undergoes constitutive endocytosis, endocytic sorting, and recycling, which delivers nutrients to the lysosomes. The receptors, along with membrane lipids, are normally returned to the plasma membrane to sustain this action. It is not known, however, whether this process is influenced by metabolic conditions. Here we report that endocytic recycling requires active mechanistic target of rapamycin (aka mammalian target of rapamycin) (mTORC1), a master metabolic sensor. Upon mTORC1 inactivation, either by starvation or by inhibitor, recycling receptors and plasma membrane lipids, such as transferrin receptors and sphingomyelin, are delivered to the lysosomes. This lysosomal targeting is independent of canonical autophagy: both WT and Atg5<sup>-/-</sup>
 mouse embryonic fibroblasts responded similarly. Furthermore, we identify hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs), an endosomal sorting complexes required for transport (ESCORT-0) component, as a downstream target of mTORC1. Hrs requires mTORC1 activity to maintain its protein expression level. Silencing Hrs without decreasing mTORC1 activity is sufficient to target transferrin and sphingomyelin to the lysosomes. It is thus evident that the canonical recycling pathway is under the regulation of mTORC1 and likely most predominant in proliferating cells where mTORC1 is highly active.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28196862</PMID>
<DateCompleted><Year>2017</Year>
<Month>06</Month>
<Day>01</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>292</Volume>
<Issue>14</Issue>
<PubDate><Year>2017</Year>
<Month>04</Month>
<Day>07</Day>
</PubDate>
</JournalIssue>
<Title>The Journal of biological chemistry</Title>
<ISOAbbreviation>J Biol Chem</ISOAbbreviation>
</Journal>
<ArticleTitle>mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.</ArticleTitle>
<Pagination><MedlinePgn>5737-5747</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M116.771451</ELocationID>
<Abstract><AbstractText>The plasma membrane of mammalian cells undergoes constitutive endocytosis, endocytic sorting, and recycling, which delivers nutrients to the lysosomes. The receptors, along with membrane lipids, are normally returned to the plasma membrane to sustain this action. It is not known, however, whether this process is influenced by metabolic conditions. Here we report that endocytic recycling requires active mechanistic target of rapamycin (aka mammalian target of rapamycin) (mTORC1), a master metabolic sensor. Upon mTORC1 inactivation, either by starvation or by inhibitor, recycling receptors and plasma membrane lipids, such as transferrin receptors and sphingomyelin, are delivered to the lysosomes. This lysosomal targeting is independent of canonical autophagy: both WT and Atg5<sup>-/-</sup>
 mouse embryonic fibroblasts responded similarly. Furthermore, we identify hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs), an endosomal sorting complexes required for transport (ESCORT-0) component, as a downstream target of mTORC1. Hrs requires mTORC1 activity to maintain its protein expression level. Silencing Hrs without decreasing mTORC1 activity is sufficient to target transferrin and sphingomyelin to the lysosomes. It is thus evident that the canonical recycling pathway is under the regulation of mTORC1 and likely most predominant in proliferating cells where mTORC1 is highly active.</AbstractText>
<CopyrightInformation>© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dauner</LastName>
<ForeName>Kristin</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eid</LastName>
<ForeName>Walaa</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Raghupathy</LastName>
<ForeName>Riya</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Presley</LastName>
<ForeName>John F</ForeName>
<Initials>JF</Initials>
<AffiliationInfo><Affiliation>the Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zha</LastName>
<ForeName>Xiaohui</ForeName>
<Initials>X</Initials>
<Identifier Source="ORCID">0000-0003-2873-3073</Identifier>
<AffiliationInfo><Affiliation>From the Chronic Disease Program, Ottawa Hospital Research Institute and xzha@ohri.ca.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1H 8L6, Canada and.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>MOP-130453</GrantID>
<Agency>CIHR</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>02</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>J Biol Chem</MedlineTA>
<NlmUniqueID>2985121R</NlmUniqueID>
<ISSNLinking>0021-9258</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495773">Atg5 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D056827">Endosomal Sorting Complexes Required for Transport</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D046912">Multiprotein Complexes</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D013109">Sphingomyelins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014168">Transferrin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001693" MajorTopicYN="N">Biological Transport, Active</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004622" MajorTopicYN="N">Embryo, Mammalian</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004705" MajorTopicYN="N">Endocytosis</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D056827" MajorTopicYN="N">Endosomal Sorting Complexes Required for Transport</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName>
<QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D046912" MajorTopicYN="N">Multiprotein Complexes</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013109" MajorTopicYN="N">Sphingomyelins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014168" MajorTopicYN="N">Transferrin</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Hrs</Keyword>
<Keyword MajorTopicYN="Y">autophagy</Keyword>
<Keyword MajorTopicYN="Y">endocytosis</Keyword>
<Keyword MajorTopicYN="Y">endosomal sorting complexes required for transport (ESCRT)</Keyword>
<Keyword MajorTopicYN="Y">lysosome</Keyword>
<Keyword MajorTopicYN="Y">mTOR complex (mTORC)</Keyword>
<Keyword MajorTopicYN="Y">membrane recycling</Keyword>
<Keyword MajorTopicYN="Y">receptor recycling</Keyword>
<Keyword MajorTopicYN="Y">transferrin</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year>
<Month>12</Month>
<Day>19</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2017</Year>
<Month>02</Month>
<Day>10</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>2</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2017</Year>
<Month>6</Month>
<Day>2</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>2</Month>
<Day>16</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">28196862</ArticleId>
<ArticleId IdType="pii">M116.771451</ArticleId>
<ArticleId IdType="doi">10.1074/jbc.M116.771451</ArticleId>
<ArticleId IdType="pmc">PMC5392569</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Nat Rev Mol Cell Biol. 2015 Aug;16(8):461-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26177004</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2014 Oct 9;159(2):242-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25303523</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2009 Mar 26;458(7237):445-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19325624</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Rep. 2012 Jan 26;1(1):29-35</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22832105</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2005 Apr;1(1):23-36</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16874023</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Rep. 2015 Sep 22;12 (11):1876-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26344761</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2013 May;14(5):283-96</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23609508</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Dev Cell. 2011 Jul 19;21(1):77-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21763610</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Biol. 1993 Jun;121(6):1257-69</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8509447</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2007 May;8(5):355-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17450176</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2014 May 1;509(7498):49-54</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24670665</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2014 Mar;15(3):155-62</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24556838</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21157483</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Cell Biol. 2011 Apr;13(4):453-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21394080</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Opin Cell Biol. 1995 Aug;7(4):552-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7495576</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2011 Jul 19;108(29):11906-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21730137</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Sci. 2013 Apr 15;126(Pt 8):1713-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23641065</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Cell Biol. 1989 Jun;108(6):2169-81</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2738091</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1991 Nov 5;266(31):21125-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1939155</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2000 May 19;275(20):15279-86</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10809763</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2012 May 02;485(7396):109-13</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22552098</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Elife. 2015 Apr 22;4:e07736</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25902403</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Cycle. 2011 May 1;10(9):1337-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21403467</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Traffic. 2012 Mar;13(3):468-82</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22118530</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>Canada</li>
</country>
<region><li>Québec</li>
</region>
<settlement><li>Montréal</li>
</settlement>
<orgName><li>Université McGill</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Dauner, Kristin" sort="Dauner, Kristin" uniqKey="Dauner K" first="Kristin" last="Dauner">Kristin Dauner</name>
<name sortKey="Raghupathy, Riya" sort="Raghupathy, Riya" uniqKey="Raghupathy R" first="Riya" last="Raghupathy">Riya Raghupathy</name>
</noCountry>
<country name="Canada"><noRegion><name sortKey="Eid, Walaa" sort="Eid, Walaa" uniqKey="Eid W" first="Walaa" last="Eid">Walaa Eid</name>
</noRegion>
<name sortKey="Presley, John F" sort="Presley, John F" uniqKey="Presley J" first="John F" last="Presley">John F. Presley</name>
<name sortKey="Zha, Xiaohui" sort="Zha, Xiaohui" uniqKey="Zha X" first="Xiaohui" last="Zha">Xiaohui Zha</name>
<name sortKey="Zha, Xiaohui" sort="Zha, Xiaohui" uniqKey="Zha X" first="Xiaohui" last="Zha">Xiaohui Zha</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000688 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000688 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:28196862
   |texte=   mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:28196862" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.

mTOR complex 1 activity is required to maintain the canonical endocytic recycling pathway against lysosomal delivery.

Source :

Descripteurs français

English descriptors

Abstract

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

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki