Full metadata record
DC Field | Value | Language |
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dc.citation.number | 14 | - |
dc.citation.startPage | 2205913 | - |
dc.citation.title | ADVANCED SCIENCE | - |
dc.citation.volume | 10 | - |
dc.contributor.author | Lee, Ah Reum | - |
dc.contributor.author | Park, Chan Young | - |
dc.date.accessioned | 2023-12-21T12:40:47Z | - |
dc.date.available | 2023-12-21T12:40:47Z | - |
dc.date.created | 2023-03-09 | - |
dc.date.issued | 2023-05 | - |
dc.description.abstract | Entosis is a non-apoptotic cell death process that forms characteristic cell-in-cell structures in cancers, killing invading cells. Intracellular Ca2+ dynamics are essential for cellular processes, including actomyosin contractility, migration, and autophagy. However, the significance of Ca2+ and Ca2+ channels participating in entosis is unclear. Here, it is shown that intracellular Ca2+ signaling regulates entosis via SEPTIN-Orai1-Ca2+/CaM-MLCK-actomyosin axis. Intracellular Ca2+ oscillations in entotic cells show spatiotemporal variations during engulfment, mediated by Orai1 Ca2+ channels in plasma membranes. SEPTIN controlled polarized distribution of Orai1 for local MLCK activation, resulting in MLC phosphorylation and actomyosin contraction, leads to internalization of invasive cells. Ca2+ chelators and SEPTIN, Orai1, and MLCK inhibitors suppress entosis. This study identifies potential targets for treating entosis-associated tumors, showing that Orai1 is an entotic Ca2+ channel that provides essential Ca2+ signaling and sheds light on the molecular mechanism underlying entosis that involves SEPTIN filaments, Orai1, and MLCK. | - |
dc.identifier.bibliographicCitation | ADVANCED SCIENCE, v.10, no.14, pp.2205913 | - |
dc.identifier.doi | 10.1002/advs.202205913 | - |
dc.identifier.issn | 2198-3844 | - |
dc.identifier.scopusid | 2-s2.0-85150993707 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/62430 | - |
dc.identifier.wosid | 000955322200001 | - |
dc.language | 영어 | - |
dc.publisher | Wiley-VCH Verlag | - |
dc.title | Orai1 is an entotic Ca2+ channel for non-apoptotic cell death, entosis in cancer development | - |
dc.type | Article | - |
dc.description.isOpenAccess | TRUE | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary;Nanoscience & Nanotechnology;Materials Science, Multidisciplinary | - |
dc.relation.journalResearchArea | Chemistry;Science & Technology - Other Topics;Materials Science | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | entosis | - |
dc.subject.keywordAuthor | Orai1 | - |
dc.subject.keywordAuthor | SEPTIN | - |
dc.subject.keywordAuthor | calcium signaling | - |
dc.subject.keywordAuthor | cell-in-cell | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.subject.keywordPlus | OSCILLATIONS | - |
dc.subject.keywordPlus | HOMEOSTASIS | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | SCREEN | - |
dc.subject.keywordPlus | EPITHELIAL BARRIER | - |
dc.subject.keywordPlus | STIM1 | - |
dc.subject.keywordPlus | STORE | - |
dc.subject.keywordPlus | SEPTINS | - |
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