RapamycinFungusV1, Main, Exploration, bibRecord, 000285

Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.

Identifieur interne : 000285 ( Main/Exploration ); précédent : 000284; suivant : 000286

Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.

Source :

Journal of molecular cell biology [ 1759-4685 ] ; 2019.

RBID : pubmed:30428057

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Animals (MeSH), Carrier Proteins (genetics), Carrier Proteins (metabolism), Cell Differentiation (MeSH), Cell Proliferation (MeSH), Glycolysis (physiology), Mechanistic Target of Rapamycin Complex 2 (metabolism), Mediator Complex Subunit 1 (metabolism), Membrane Proteins (metabolism), Mice (MeSH), Mice, Transgenic (MeSH), T-Lymphocytes (metabolism), TOR Serine-Threonine Kinases (metabolism), Thyroid Hormones (metabolism).
MESH :
- chemical , genetics : Carrier Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Carrier Proteins, Mechanistic Target of Rapamycin Complex 2, Mediator Complex Subunit 1, Membrane Proteins, TOR Serine-Threonine Kinases, Thyroid Hormones.
- metabolism : T-Lymphocytes.
- physiology : Glycolysis.
- Animals, Cell Differentiation, Cell Proliferation, Mice, Mice, Transgenic.

Abstract

Glucose metabolism plays a key role in thymocyte development. The mammalian target of rapamycin complex 2 (mTORC2) is a critical regulator of cell growth and metabolism, but its role in early thymocyte development and metabolism has not been fully studied. We show here that genetic ablation of Sin1, an essential component of mTORC2, in T lineage cells results in severely impaired thymocyte development at the CD4-CD8- double negative (DN) stages but not at the CD4+CD8+ double positive (DP) or later stages. Notably, Sin1-deficient DN thymocytes show markedly reduced proliferation and glycolysis. Importantly, we discover that the M2 isoform of pyruvate kinase (PKM2) is a novel and crucial Sin1 effector in promoting DN thymocyte development and metabolism. At the molecular level, we show that Sin1-mTORC2 controls PKM2 expression through an AKT-dependent PPAR-γ nuclear translocation. Together, our study unravels a novel mTORC2-PPAR-γ-PKM2 pathway in immune-metabolic regulation of early thymocyte development.

DOI: 10.1093/jmcb/mjy065
PubMed: 30428057
PubMed Central: PMC6392101

Affiliations:

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

to stream Main, to step Corpus: 000406
to stream Main, to step Curation: 000406

Le document en format XML

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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Sun, Hongxiang" sort="Sun, Hongxiang" uniqKey="Sun H" first="Hongxiang" last="Sun">Hongxiang Sun</name>
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<author><name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
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<author><name sortKey="Chen, Lei" sort="Chen, Lei" uniqKey="Chen L" first="Lei" last="Chen">Lei Chen</name>
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<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.</title>
<author><name sortKey="Ouyang, Xinxing" sort="Ouyang, Xinxing" uniqKey="Ouyang X" first="Xinxing" last="Ouyang">Xinxing Ouyang</name>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Han, Yuheng" sort="Han, Yuheng" uniqKey="Han Y" first="Yuheng" last="Han">Yuheng Han</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea>
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<author><name sortKey="Qu, Guojun" sort="Qu, Guojun" uniqKey="Qu G" first="Guojun" last="Qu">Guojun Qu</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Wu, Ningbo" sort="Wu, Ningbo" uniqKey="Wu N" first="Ningbo" last="Wu">Ningbo Wu</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Liu, Hongzhi" sort="Liu, Hongzhi" uniqKey="Liu H" first="Hongzhi" last="Liu">Hongzhi Liu</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
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<author><name sortKey="Arojo, Omotooke" sort="Arojo, Omotooke" uniqKey="Arojo O" first="Omotooke" last="Arojo">Omotooke Arojo</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Immunobiology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, 333 Cedar Street, New Haven, CT</wicri:regionArea>
<placeName><region type="state">Connecticut</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sun, Hongxiang" sort="Sun, Hongxiang" uniqKey="Sun H" first="Hongxiang" last="Sun">Hongxiang Sun</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea>
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<author><name sortKey="Liu, Xiaobo" sort="Liu, Xiaobo" uniqKey="Liu X" first="Xiaobo" last="Liu">Xiaobo Liu</name>
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<author><name sortKey="Liu, Dou" sort="Liu, Dou" uniqKey="Liu D" first="Dou" last="Liu">Dou Liu</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Immunobiology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, 333 Cedar Street, New Haven, CT</wicri:regionArea>
<placeName><region type="state">Connecticut</region>
</placeName>
</affiliation>
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<author><name sortKey="Chen, Lei" sort="Chen, Lei" uniqKey="Chen L" first="Lei" last="Chen">Lei Chen</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
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<author><name sortKey="Zou, Qiang" sort="Zou, Qiang" uniqKey="Zou Q" first="Qiang" last="Zou">Qiang Zou</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai</wicri:regionArea>
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<author><name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
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</placeName>
</affiliation>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Cell Differentiation (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Glycolysis (physiology)</term>
<term>Mechanistic Target of Rapamycin Complex 2 (metabolism)</term>
<term>Mediator Complex Subunit 1 (metabolism)</term>
<term>Membrane Proteins (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>T-Lymphocytes (metabolism)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Thyroid Hormones (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Complexe-2 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Différenciation cellulaire (MeSH)</term>
<term>Glycolyse (physiologie)</term>
<term>Hormones thyroïdiennes (métabolisme)</term>
<term>Lymphocytes T (métabolisme)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (métabolisme)</term>
<term>Protéines membranaires (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>Sous-unité-1 du complexe médiateur (métabolisme)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Carrier Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>Carrier Proteins</term>
<term>Mechanistic Target of Rapamycin Complex 2</term>
<term>Mediator Complex Subunit 1</term>
<term>Membrane Proteins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Thyroid Hormones</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéines de transport</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complexe-2 cible mécanistique de la rapamycine</term>
<term>Hormones thyroïdiennes</term>
<term>Lymphocytes T</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Protéines de transport</term>
<term>Protéines membranaires</term>
<term>Sous-unité-1 du complexe médiateur</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Cell Differentiation</term>
<term>Cell Proliferation</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Différenciation cellulaire</term>
<term>Prolifération cellulaire</term>
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<front><div type="abstract" xml:lang="en">Glucose metabolism plays a key role in thymocyte development. The mammalian target of rapamycin complex 2 (mTORC2) is a critical regulator of cell growth and metabolism, but its role in early thymocyte development and metabolism has not been fully studied. We show here that genetic ablation of Sin1, an essential component of mTORC2, in T lineage cells results in severely impaired thymocyte development at the CD4-CD8- double negative (DN) stages but not at the CD4+CD8+ double positive (DP) or later stages. Notably, Sin1-deficient DN thymocytes show markedly reduced proliferation and glycolysis. Importantly, we discover that the M2 isoform of pyruvate kinase (PKM2) is a novel and crucial Sin1 effector in promoting DN thymocyte development and metabolism. At the molecular level, we show that Sin1-mTORC2 controls PKM2 expression through an AKT-dependent PPAR-γ nuclear translocation. Together, our study unravels a novel mTORC2-PPAR-γ-PKM2 pathway in immune-metabolic regulation of early thymocyte development.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30428057</PMID>
<DateCompleted><Year>2020</Year>
<Month>06</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>06</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1759-4685</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>11</Volume>
<Issue>2</Issue>
<PubDate><Year>2019</Year>
<Month>02</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Journal of molecular cell biology</Title>
<ISOAbbreviation>J Mol Cell Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.</ArticleTitle>
<Pagination><MedlinePgn>93-106</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1093/jmcb/mjy065</ELocationID>
<Abstract><AbstractText>Glucose metabolism plays a key role in thymocyte development. The mammalian target of rapamycin complex 2 (mTORC2) is a critical regulator of cell growth and metabolism, but its role in early thymocyte development and metabolism has not been fully studied. We show here that genetic ablation of Sin1, an essential component of mTORC2, in T lineage cells results in severely impaired thymocyte development at the CD4-CD8- double negative (DN) stages but not at the CD4+CD8+ double positive (DP) or later stages. Notably, Sin1-deficient DN thymocytes show markedly reduced proliferation and glycolysis. Importantly, we discover that the M2 isoform of pyruvate kinase (PKM2) is a novel and crucial Sin1 effector in promoting DN thymocyte development and metabolism. At the molecular level, we show that Sin1-mTORC2 controls PKM2 expression through an AKT-dependent PPAR-γ nuclear translocation. Together, our study unravels a novel mTORC2-PPAR-γ-PKM2 pathway in immune-metabolic regulation of early thymocyte development.</AbstractText>
<CopyrightInformation>© The Author(s) (2019). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ouyang</LastName>
<ForeName>Xinxing</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Han</LastName>
<ForeName>Yuheng</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qu</LastName>
<ForeName>Guojun</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Man</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Ningbo</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Hongzhi</ForeName>
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<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
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<ForeName>Omotooke</ForeName>
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<AffiliationInfo><Affiliation>Department of Immunobiology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Hongxiang</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Xiaobo</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Dou</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Immunobiology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Lei</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zou</LastName>
<ForeName>Qiang</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Su</LastName>
<ForeName>Bing</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Shanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Immunobiology and the Vascular Biology and Therapeutics Program, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, USA.</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>
</Article>
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<MedlineTA>J Mol Cell Biol</MedlineTA>
<NlmUniqueID>101503669</NlmUniqueID>
<ISSNLinking>1759-4685</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D056913">Mediator Complex Subunit 1</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance>
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<NameOfSubstance UI="C561937">stress-activated protein kinase-interacting protein, mouse</NameOfSubstance>
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<NameOfSubstance UI="C053648">thyroid hormone-binding proteins</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D056913" MajorTopicYN="N">Mediator Complex Subunit 1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013963" MajorTopicYN="N">Thyroid Hormones</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">PKM2</Keyword>
<Keyword MajorTopicYN="Y">PPAR-γ</Keyword>
<Keyword MajorTopicYN="Y">Sin1</Keyword>
<Keyword MajorTopicYN="Y">mTORC2</Keyword>
<Keyword MajorTopicYN="Y">metabolism</Keyword>
<Keyword MajorTopicYN="Y">thymocyte development</Keyword>
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<Month>10</Month>
<Day>16</Day>
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<affiliations><list><country><li>République populaire de Chine</li>
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<name sortKey="Li, Man" sort="Li, Man" uniqKey="Li M" first="Man" last="Li">Man Li</name>
<name sortKey="Liu, Hongzhi" sort="Liu, Hongzhi" uniqKey="Liu H" first="Hongzhi" last="Liu">Hongzhi Liu</name>
<name sortKey="Liu, Xiaobo" sort="Liu, Xiaobo" uniqKey="Liu X" first="Xiaobo" last="Liu">Xiaobo Liu</name>
<name sortKey="Qu, Guojun" sort="Qu, Guojun" uniqKey="Qu G" first="Guojun" last="Qu">Guojun Qu</name>
<name sortKey="Su, Bing" sort="Su, Bing" uniqKey="Su B" first="Bing" last="Su">Bing Su</name>
<name sortKey="Sun, Hongxiang" sort="Sun, Hongxiang" uniqKey="Sun H" first="Hongxiang" last="Sun">Hongxiang Sun</name>
<name sortKey="Wu, Ningbo" sort="Wu, Ningbo" uniqKey="Wu N" first="Ningbo" last="Wu">Ningbo Wu</name>
<name sortKey="Zou, Qiang" sort="Zou, Qiang" uniqKey="Zou Q" first="Qiang" last="Zou">Qiang Zou</name>
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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

Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.

Metabolic regulation of T cell development by Sin1-mTORC2 is mediated by pyruvate kinase M2.

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