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STIM1 knock-down decreases the affinity of obinutuzumab for CD20 by altering CD20 localization to Triton-soluble membrane
DC Field | Value | Language |
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dc.contributor.author | 김주영 | - |
dc.date.accessioned | 2020-09-29T01:13:28Z | - |
dc.date.available | 2020-09-29T01:13:28Z | - |
dc.date.issued | 2020-06 | - |
dc.identifier.issn | 0009-9104 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/179445 | - |
dc.description.abstract | Obinutuzumab is thought to exert its effects through its high antibody-dependent cellular cytotoxicity (ADCC) via glyco-engineering of the Fc region. In addition, obinutuzumab causes direct binding-induced cell death (DCD) only by specifically binding to its target CD20, a Ca2+ channel. However, the specific features of CD20 related to obinutuzumab binding-induction of cell death are not clearly understood. In this study, we evaluated the relationship between the Ca2+ channel features of CD20 as a store-operated Ca2+ channel (SOC) and obinutuzumab binding-induced cell death. Ca2+ channel function and biochemical analysis revealed that CD20 is an Orai1- and stromal interaction molecule (STIM1)-dependent Ca2+ pore. However, binding of obinutuzumab on CD20 did not have any effect on Ca2+ influx activity of CD20; the direct cell death rate mediated by obinutuzumab binding was almost equivalent with or without the extracellular Ca2+ condition. Given the apparent interaction between STIM1 and CD20, we observed Triton-X solubilized obinutuzumab-bound CD20 accompanied by STIM1. Subsequently, obinutuzumab binding and cell death were decreased by STIM1 knock-down in Ramos B cells. Thus, STIM1 directly contributes to cell death by increasing the affinity of cells for obinutuzumab by transferring CD20 to the Triton-soluble membrane region. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Blackwell Scientific Publications | - |
dc.relation.isPartOf | CLINICAL AND EXPERIMENTAL IMMUNOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | STIM1 knock-down decreases the affinity of obinutuzumab for CD20 by altering CD20 localization to Triton-soluble membrane | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pharmacology (약리학교실) | - |
dc.contributor.googleauthor | W Heo | - |
dc.contributor.googleauthor | N Jin | - |
dc.contributor.googleauthor | M S Park | - |
dc.contributor.googleauthor | H-Y Kim | - |
dc.contributor.googleauthor | S M Yoon | - |
dc.contributor.googleauthor | J Lee | - |
dc.contributor.googleauthor | J Y Kim | - |
dc.identifier.doi | 10.1111/cei.13427 | - |
dc.contributor.localId | A00942 | - |
dc.relation.journalcode | J00550 | - |
dc.identifier.eissn | 1365-2249 | - |
dc.identifier.pmid | 32056202 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/full/10.1111/cei.13427 | - |
dc.subject.keyword | CD20 | - |
dc.subject.keyword | Ca2+ | - |
dc.subject.keyword | STIM1 | - |
dc.subject.keyword | direct binding-induced cell death | - |
dc.subject.keyword | obinutuzumab | - |
dc.subject.keyword | raft | - |
dc.contributor.alternativeName | Kim, Joo Young | - |
dc.contributor.affiliatedAuthor | 김주영 | - |
dc.citation.volume | 200 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 260 | - |
dc.citation.endPage | 271 | - |
dc.identifier.bibliographicCitation | CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol.200(3) : 260-271, 2020-06 | - |
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