ASCT2 (SLC1A5)-Deficient Mice Have Normal B-cells Developments, proliferation, and Antibody Production

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dc.authoridYabas, Mehmet/0000-0002-3462-5389
dc.authoridEnders, Anselm/0000-0001-5933-6463
dc.authoridMasle-Farquhar, Etienne/0000-0001-9355-8027
dc.authoridBroer, Stefan/0000-0002-8040-1634
dc.authorwosidYabas, Mehmet/D-9513-2012
dc.authorwosidEnders, Anselm/B-1165-2011
dc.authorwosidBroer, Stefan/A-1286-2008
dc.contributor.authorMasle-Farquhar, Etienne
dc.contributor.authorBroer, Angelika
dc.contributor.authorYabas, Mehmet
dc.contributor.authorEnders, Anselm
dc.contributor.authorBroer, Stefan
dc.date.accessioned2024-06-12T11:14:12Z
dc.date.available2024-06-12T11:14:12Z
dc.date.issued2017
dc.departmentTrakya Üniversitesien_US
dc.description.abstractSLC1A5 (solute carrier family 1, member 5) is a small neutral amino acid exchanger that is upregulated in rapidly proliferating lymphocytes but also in many primary human cancers. Furthermore, cancer cell lines have been shown to require SLC1A5 for their survival in vitro. One of SLC1A5's primary substrates is the immunomodulatory amino acid glutamine, which plays an important role in multiple key processes, such as energy supply, macromolecular synthesis, nucleotide biosynthesis, redox homeostasis, and resistance against oxidative stress. These processes are also essential to immune cells, including neutrophils, macrophages, B and T lymphocytes. We show here that mice with a stop codon in Slc1a5 have reduced glutamine uptake in activated lymphocytes and primary fibroblasts. B and T cell populations and maturation in resting mice were not affected by absence of SLC1A5. Antibody production in resting and immunized mice and the germinal center response to immunization were also found to be normal. SLC1A5 has been recently described as a novel target for the treatment of a variety of cancers, and our results indicate that inhibition of SLC1A5 in cancer therapy may be tolerated well by the immune system of cancer patients.en_US
dc.description.sponsorshipAustralian National Health and Medical Research Council [1105857]; Career Development Fellowship [1035858]; National Health and Medical Research Council of Australia [1105857] Funding Source: NHMRCen_US
dc.description.sponsorshipThis work was supported by Australian National Health and Medical Research Council Grant 1105857 (SB) and Career Development Fellowship 1035858 (AE).en_US
dc.identifier.doi10.3389/fimmu.2017.00549
dc.identifier.issn1664-3224
dc.identifier.pmid28553292en_US
dc.identifier.urihttps://doi.org/10.3389/fimmu.2017.00549
dc.identifier.urihttps://hdl.handle.net/20.500.14551/23845
dc.identifier.volume8en_US
dc.identifier.wosWOS:000401041700002en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherFrontiers Media Saen_US
dc.relation.ispartofFrontiers In Immunologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectSLC1A5en_US
dc.subjectGlutamineen_US
dc.subjectB Cellsen_US
dc.subjectGlutaminolysisen_US
dc.subjectASC T2en_US
dc.subjectGlutamine Uptakeen_US
dc.subjectAmino-Acid Transportersen_US
dc.subjectGlutamine Uptakeen_US
dc.subjectMetabolic Pathwaysen_US
dc.subjectStem-Cellsen_US
dc.subjectCanceren_US
dc.subjectExpressionen_US
dc.subjectGlucoseen_US
dc.subjectGrowthen_US
dc.subjectInhibitionen_US
dc.subjectSurvivalen_US
dc.titleASCT2 (SLC1A5)-Deficient Mice Have Normal B-cells Developments, proliferation, and Antibody Productionen_US
dc.typeArticleen_US

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