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CD20/TNFR1 dual-targeting antibody enhances lysosome rupture-mediated cell death in B cell lymphoma
DC Field | Value | Language |
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dc.contributor.author | 김주영 | - |
dc.date.accessioned | 2024-03-22T05:47:16Z | - |
dc.date.available | 2024-03-22T05:47:16Z | - |
dc.date.issued | 2023-06 | - |
dc.identifier.issn | 0340-7004 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/198205 | - |
dc.description.abstract | Obinutuzumab is a therapeutic antibody for B cell non-Hodgkin’s Lymphoma (BNHL), which is a glyco-engineered anti-CD20 antibody with enhanced antibody-dependent cellular cytotoxicity (ADCC) and causes binding-induced direct cell death (DCD) through lysosome membrane permeabilization (LMP). Tumour necrosis factor receptor 1 (TNFR1), a pro-inflammatory death receptor, also evokes cell death, partly through lysosomal rupture. As both obinutuzumab- and TNFR1-induced cell deaths are mediated by LMP and combining TNFR1 and obinutuzumab can amplify LMP-mediated cell death, we made dual-targeting antibody for CD20 and TNFR1 to enhance DCD of obinutuzumab. Obinutuzumab treatment-induced CD20 and TNFR1 colocalisation, and TNFR1-overexpressing cells showed increased obinutuzumab-induced DCD. Two targeting modes, anti-CD20/TNFR1 bispecific antibodies (bsAbs), and obinutuzumab-TNFα fusion proteins (OBI-TNFα | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Springer Verlag | - |
dc.relation.isPartOf | CANCER IMMUNOLOGY IMMUNOTHERAPY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.subject.MESH | Antibodies, Bispecific / pharmacology | - |
dc.subject.MESH | Antigens, CD20 | - |
dc.subject.MESH | Cell Death | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Lymphoma, B-Cell* / drug therapy | - |
dc.subject.MESH | Receptors, Tumor Necrosis Factor, Type I / therapeutic use | - |
dc.subject.MESH | Tumor Necrosis Factor-alpha* | - |
dc.title | CD20/TNFR1 dual-targeting antibody enhances lysosome rupture-mediated cell death in B cell lymphoma | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pharmacology (약리학교실) | - |
dc.contributor.googleauthor | Jeong Ryeol Kim | - |
dc.contributor.googleauthor | Donghyuk Lee | - |
dc.contributor.googleauthor | Yerim Kim 1, Joo Young Kim | - |
dc.identifier.doi | 10.1007/s00262-022-03344-9 | - |
dc.contributor.localId | A00942 | - |
dc.relation.journalcode | J00445 | - |
dc.identifier.eissn | 1432-0851 | - |
dc.identifier.pmid | 36534148 | - |
dc.identifier.url | https://link.springer.com/article/10.1007/s00262-022-03344-9 | - |
dc.subject.keyword | Antibody binding-induced cell death | - |
dc.subject.keyword | BNHL (B cell non-Hodgkin’s lymphoma) | - |
dc.subject.keyword | Bispecific or fusion proteins | - |
dc.subject.keyword | Obinutuzumab | - |
dc.subject.keyword | TNFR1 | - |
dc.contributor.alternativeName | Kim, Joo Young | - |
dc.contributor.affiliatedAuthor | 김주영 | - |
dc.citation.volume | 72 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1567 | - |
dc.citation.endPage | 1580 | - |
dc.identifier.bibliographicCitation | CANCER IMMUNOLOGY IMMUNOTHERAPY, Vol.72(6) : 1567-1580, 2023-06 | - |
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