Interleukin-18 up-regulates amino acid transporters and facilitates amino acid-induced mTORC1 activation in natural killer cells.
Identifieur interne : 000312 ( Main/Exploration ); précédent : 000311; suivant : 000313Interleukin-18 up-regulates amino acid transporters and facilitates amino acid-induced mTORC1 activation in natural killer cells.
Auteurs : Saeedah Musaed Almutairi [Canada, Arabie saoudite] ; Alaa Kassim Ali [Canada] ; William He [Canada] ; Doo-Seok Yang [Canada] ; Peyman Ghorbani [Canada] ; Lisheng Wang [Canada] ; Morgan D. Fullerton [Canada] ; Seung-Hwan Lee [Canada]Source :
- The Journal of biological chemistry [ 1083-351X ] ; 2019.
Descripteurs français
- KwdFr :
- Acides aminés (métabolisme), Animaux (MeSH), Antigènes CD98 (métabolisme), Cellules cultivées (MeSH), Cellules tueuses naturelles (métabolisme), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Interleukine-18 (physiologie), Prolifération cellulaire (MeSH), Régulation positive (physiologie), Souris (MeSH), Souris de lignée C57BL (MeSH).
- MESH :
English descriptors
- KwdEn :
- Amino Acids (metabolism), Animals (MeSH), Cell Proliferation (MeSH), Cells, Cultured (MeSH), Fusion Regulatory Protein-1 (metabolism), Interleukin-18 (physiology), Killer Cells, Natural (metabolism), Mechanistic Target of Rapamycin Complex 1 (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Up-Regulation (physiology).
- MESH :
- chemical , metabolism : Amino Acids, Fusion Regulatory Protein-1, Mechanistic Target of Rapamycin Complex 1.
- chemical , physiology : Interleukin-18.
- metabolism : Killer Cells, Natural.
- physiology : Up-Regulation.
- Animals, Cell Proliferation, Cells, Cultured, Mice, Mice, Inbred C57BL.
Abstract
Upon inflammation, natural killer (NK) cells undergo metabolic changes to support their high energy demand for effector function and proliferation. The metabolic changes are usually accompanied by an increase in the expression of nutrient transporters, leading to increased nutrient uptake. Among various cytokines inducing NK cell proliferation, the mechanisms underlying the effect of interleukin (IL)-18 in promoting NK cell proliferation are not completely understood. Here, we demonstrate that IL-18 is a potent cytokine that can enhance the expression of the nutrient transporter CD98/LAT1 for amino acids independently of the mTORC1 pathway and thereby induce a dramatic metabolic change associated with increased proliferation of NK cells. Notably, treatment of IL-18-stimulated NK cells with leucine activates the metabolic sensor mTORC1, indicating that the high expression of amino acid transporters induces amino acid-driven mTORC1 activation. Inhibition of the amino acid transporter CD98/LAT1 abrogated the leucine-driven mTORC1 activation and reduced NK cell effector function. Taken together, our study identified a novel role of IL-18 in up-regulating nutrient transporters on NK cells and thereby inducing metabolic changes, including the mTORC1 activation by amino acids.
DOI: 10.1074/jbc.RA118.005892
PubMed: 30696773
PubMed Central: PMC6433059
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interleukin-18 up-regulates amino acid transporters and facilitates amino acid-induced mTORC1 activation in natural killer cells.</title><author><name sortKey="Almutairi, Saeedah Musaed" sort="Almutairi, Saeedah Musaed" uniqKey="Almutairi S" first="Saeedah Musaed" last="Almutairi">Saeedah Musaed Almutairi</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Botany and Microbiology Department, College of Sciences, King Saud University, Riyadh 11451, Saudi Arabia.</nlm:affiliation><country xml:lang="fr">Arabie saoudite</country><wicri:regionArea>Botany and Microbiology Department, College of Sciences, King Saud University, Riyadh 11451</wicri:regionArea><wicri:noRegion>Riyadh 11451</wicri:noRegion></affiliation></author><author><name sortKey="Ali, Alaa Kassim" sort="Ali, Alaa Kassim" uniqKey="Ali A" first="Alaa Kassim" last="Ali">Alaa Kassim Ali</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="He, William" sort="He, William" uniqKey="He W" first="William" last="He">William He</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Doo Seok" sort="Yang, Doo Seok" uniqKey="Yang D" first="Doo-Seok" last="Yang">Doo-Seok Yang</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Ghorbani, Peyman" sort="Ghorbani, Peyman" uniqKey="Ghorbani P" first="Peyman" last="Ghorbani">Peyman Ghorbani</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Lisheng" sort="Wang, Lisheng" uniqKey="Wang L" first="Lisheng" last="Wang">Lisheng Wang</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Fullerton, Morgan D" sort="Fullerton, Morgan D" uniqKey="Fullerton M" first="Morgan D" last="Fullerton">Morgan D. Fullerton</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Seung Hwan" sort="Lee, Seung Hwan" uniqKey="Lee S" first="Seung-Hwan" last="Lee">Seung-Hwan Lee</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and seunglee@uottawa.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:30696773</idno><idno type="pmid">30696773</idno><idno type="doi">10.1074/jbc.RA118.005892</idno><idno type="pmc">PMC6433059</idno><idno type="wicri:Area/Main/Corpus">000357</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000357</idno><idno type="wicri:Area/Main/Curation">000357</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000357</idno><idno type="wicri:Area/Main/Exploration">000357</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Interleukin-18 up-regulates amino acid transporters and facilitates amino acid-induced mTORC1 activation in natural killer cells.</title><author><name sortKey="Almutairi, Saeedah Musaed" sort="Almutairi, Saeedah Musaed" uniqKey="Almutairi S" first="Saeedah Musaed" last="Almutairi">Saeedah Musaed Almutairi</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Botany and Microbiology Department, College of Sciences, King Saud University, Riyadh 11451, Saudi Arabia.</nlm:affiliation><country xml:lang="fr">Arabie saoudite</country><wicri:regionArea>Botany and Microbiology Department, College of Sciences, King Saud University, Riyadh 11451</wicri:regionArea><wicri:noRegion>Riyadh 11451</wicri:noRegion></affiliation></author><author><name sortKey="Ali, Alaa Kassim" sort="Ali, Alaa Kassim" uniqKey="Ali A" first="Alaa Kassim" last="Ali">Alaa Kassim Ali</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="He, William" sort="He, William" uniqKey="He W" first="William" last="He">William He</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Yang, Doo Seok" sort="Yang, Doo Seok" uniqKey="Yang D" first="Doo-Seok" last="Yang">Doo-Seok Yang</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Ghorbani, Peyman" sort="Ghorbani, Peyman" uniqKey="Ghorbani P" first="Peyman" last="Ghorbani">Peyman Ghorbani</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Lisheng" sort="Wang, Lisheng" uniqKey="Wang L" first="Lisheng" last="Wang">Lisheng Wang</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Fullerton, Morgan D" sort="Fullerton, Morgan D" uniqKey="Fullerton M" first="Morgan D" last="Fullerton">Morgan D. Fullerton</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</nlm:affiliation><country>Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Seung Hwan" sort="Lee, Seung Hwan" uniqKey="Lee S" first="Seung-Hwan" last="Lee">Seung-Hwan Lee</name><affiliation wicri:level="1"><nlm:affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and seunglee@uottawa.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5</wicri:regionArea><wicri:noRegion>Ontario K1H 8M5</wicri:noRegion></affiliation></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="eISSN">1083-351X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acids (metabolism)</term><term>Animals (MeSH)</term><term>Cell Proliferation (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Fusion Regulatory Protein-1 (metabolism)</term><term>Interleukin-18 (physiology)</term><term>Killer Cells, Natural (metabolism)</term><term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Up-Regulation (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acides aminés (métabolisme)</term><term>Animaux (MeSH)</term><term>Antigènes CD98 (métabolisme)</term><term>Cellules cultivées (MeSH)</term><term>Cellules tueuses naturelles (métabolisme)</term><term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term><term>Interleukine-18 (physiologie)</term><term>Prolifération cellulaire (MeSH)</term><term>Régulation positive (physiologie)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amino Acids</term><term>Fusion Regulatory Protein-1</term><term>Mechanistic Target of Rapamycin Complex 1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Interleukin-18</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Killer Cells, Natural</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acides aminés</term><term>Antigènes CD98</term><term>Cellules tueuses naturelles</term><term>Complexe-1 cible mécanistique de la rapamycine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Interleukine-18</term><term>Régulation positive</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Proliferation</term><term>Cells, Cultured</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Prolifération cellulaire</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Upon inflammation, natural killer (NK) cells undergo metabolic changes to support their high energy demand for effector function and proliferation. The metabolic changes are usually accompanied by an increase in the expression of nutrient transporters, leading to increased nutrient uptake. Among various cytokines inducing NK cell proliferation, the mechanisms underlying the effect of interleukin (IL)-18 in promoting NK cell proliferation are not completely understood. Here, we demonstrate that IL-18 is a potent cytokine that can enhance the expression of the nutrient transporter CD98/LAT1 for amino acids independently of the mTORC1 pathway and thereby induce a dramatic metabolic change associated with increased proliferation of NK cells. Notably, treatment of IL-18-stimulated NK cells with leucine activates the metabolic sensor mTORC1, indicating that the high expression of amino acid transporters induces amino acid-driven mTORC1 activation. Inhibition of the amino acid transporter CD98/LAT1 abrogated the leucine-driven mTORC1 activation and reduced NK cell effector function. Taken together, our study identified a novel role of IL-18 in up-regulating nutrient transporters on NK cells and thereby inducing metabolic changes, including the mTORC1 activation by amino acids.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30696773</PMID><DateCompleted><Year>2019</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>294</Volume><Issue>12</Issue><PubDate><Year>2019</Year><Month>03</Month><Day>22</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Interleukin-18 up-regulates amino acid transporters and facilitates amino acid-induced mTORC1 activation in natural killer cells.</ArticleTitle><Pagination><MedlinePgn>4644-4655</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.RA118.005892</ELocationID><Abstract><AbstractText>Upon inflammation, natural killer (NK) cells undergo metabolic changes to support their high energy demand for effector function and proliferation. The metabolic changes are usually accompanied by an increase in the expression of nutrient transporters, leading to increased nutrient uptake. Among various cytokines inducing NK cell proliferation, the mechanisms underlying the effect of interleukin (IL)-18 in promoting NK cell proliferation are not completely understood. Here, we demonstrate that IL-18 is a potent cytokine that can enhance the expression of the nutrient transporter CD98/LAT1 for amino acids independently of the mTORC1 pathway and thereby induce a dramatic metabolic change associated with increased proliferation of NK cells. Notably, treatment of IL-18-stimulated NK cells with leucine activates the metabolic sensor mTORC1, indicating that the high expression of amino acid transporters induces amino acid-driven mTORC1 activation. Inhibition of the amino acid transporter CD98/LAT1 abrogated the leucine-driven mTORC1 activation and reduced NK cell effector function. Taken together, our study identified a novel role of IL-18 in up-regulating nutrient transporters on NK cells and thereby inducing metabolic changes, including the mTORC1 activation by amino acids.</AbstractText><CopyrightInformation>© 2019 Almutairi et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Almutairi</LastName><ForeName>Saeedah Musaed</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Botany and Microbiology Department, College of Sciences, King Saud University, Riyadh 11451, Saudi Arabia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ali</LastName><ForeName>Alaa Kassim</ForeName><Initials>AK</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>William</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Doo-Seok</ForeName><Initials>DS</Initials><Identifier Source="ORCID">0000-0001-8420-6302</Identifier><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghorbani</LastName><ForeName>Peyman</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Lisheng</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fullerton</LastName><ForeName>Morgan D</ForeName><Initials>MD</Initials><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung-Hwan</ForeName><Initials>SH</Initials><Identifier Source="ORCID">0000-0001-7703-6421</Identifier><AffiliationInfo><Affiliation>From the Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada and seunglee@uottawa.ca.</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>01</Month><Day>29</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="D000596">Amino Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D027261">Fusion Regulatory Protein-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020382">Interleukin-18</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="D000596" MajorTopicYN="N">Amino Acids</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D027261" MajorTopicYN="N">Fusion Regulatory Protein-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020382" MajorTopicYN="N">Interleukin-18</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007694" MajorTopicYN="N">Killer Cells, Natural</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">amino acid</Keyword><Keyword MajorTopicYN="Y">cell metabolism</Keyword><Keyword MajorTopicYN="Y">cell proliferation</Keyword><Keyword MajorTopicYN="Y">interleukin-18 (IL-18)</Keyword><Keyword MajorTopicYN="Y">mTORC1</Keyword><Keyword MajorTopicYN="Y">mammalian target of rapamycin (mTOR)</Keyword><Keyword MajorTopicYN="Y">natural killer cells (NK cells)</Keyword><Keyword MajorTopicYN="Y">nutrient uptake</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>09</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>01</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>1</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>12</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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