ATP11C promotes the differentiation of pre-B cells into immature B cells but does not affect their IL-7-dependent proliferation

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dc.authoridYabas, Mehmet/0000-0002-3462-5389
dc.authorwosidYabas, Mehmet/D-9513-2012
dc.contributor.authorYabas, Mehmet
dc.contributor.authorBostanci, Ayten
dc.contributor.authorAral, Seda
dc.date.accessioned2024-06-12T10:52:48Z
dc.date.available2024-06-12T10:52:48Z
dc.date.issued2023
dc.departmentTrakya Üniversitesien_US
dc.description.abstractThe P4-type ATPases are believed to function as flippases that contribute to the organization of the asymmetric aminophospholipid distribution on the plasma membranes of eukaryotes by their ability to internalize specific phospholipids from the outer leaflet to the inner leaflet. Despite the existence of 14 members of the P4-type ATPases in humans and 15 in mice, their roles in the immune system have not been fully understood. So far, ATP11C was shown to be important for B cells, and mice deficient for ATP11C had a developmental arrest at the pro-B to pre-B cell transition stage of B cell development. Using an ATP11C-deficient pre-B cell line generated through CRISPR/Cas9 engineering, we here tested the role of ATP11C in pre-B cells in vitro and showed that ablation of ATP11C in pre-B cells causes a defect in the flippase activity. We further demonstrated that loss of ATP11C does not impede the proliferation of pre-B cells in response to IL-7. However, pre-B cells lacking ATP11C failed to differentiate into immature B cells upon removal of IL-7. These results suggest that disruption of lipid asymmetry by loss of ATP11C in pre-B cells may control the switch from proliferation to differentiation in pre-B cells.en_US
dc.description.sponsorshipTrakya University Scientific Research Projects Coordination Unit [2019/280]en_US
dc.description.sponsorshipThis study was supported by the Trakya University Scientific Research Projects Coordination Unit (Project Number 2019/280).en_US
dc.identifier.doi10.1007/s12026-023-09364-6
dc.identifier.endpage616en_US
dc.identifier.issn0257-277X
dc.identifier.issn1559-0755
dc.identifier.issue4en_US
dc.identifier.pmid36753036en_US
dc.identifier.scopus2-s2.0-85147693751en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage609en_US
dc.identifier.urihttps://doi.org/10.1007/s12026-023-09364-6
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18840
dc.identifier.volume71en_US
dc.identifier.wosWOS:000929259800001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofImmunologic Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectATP11Cen_US
dc.subjectB Cellsen_US
dc.subjectFlippaseen_US
dc.subjectImmunologyen_US
dc.subjectPre-B Cellsen_US
dc.subjectPhospholipid Flippaseen_US
dc.subjectDeficienten_US
dc.subjectIl-7en_US
dc.subjectPhosphatidylserineen_US
dc.subjectProteinen_US
dc.subjectMiceen_US
dc.subjectTransitionen_US
dc.subjectCheckpointen_US
dc.subjectExpansionen_US
dc.subjectMouseen_US
dc.titleATP11C promotes the differentiation of pre-B cells into immature B cells but does not affect their IL-7-dependent proliferationen_US
dc.typeArticleen_US

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