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ScharerDavid Orlando

Scharer, Orlando D.
Schärer Lab.
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dc.citation.number 1 -
dc.citation.startPage 5495 -
dc.citation.title NATURE COMMUNICATIONS -
dc.citation.volume 11 -
dc.contributor.author Rageul, Julie -
dc.contributor.author Park, Jennifer J. -
dc.contributor.author Zeng, Ping Ping -
dc.contributor.author Lee, Eun-A -
dc.contributor.author Yang, Jihyeon -
dc.contributor.author Hwang, Sunyoung -
dc.contributor.author Lo, Natalie -
dc.contributor.author Weinheimer, Alexandra S. -
dc.contributor.author Scharer, Orlando D. -
dc.contributor.author Yeo, Jung-Eun -
dc.contributor.author Kim, Hyungjin -
dc.date.accessioned 2023-12-21T16:47:04Z -
dc.date.available 2023-12-21T16:47:04Z -
dc.date.created 2021-01-21 -
dc.date.issued 2020-10 -
dc.description.abstract Protecting replication fork integrity during DNA replication is essential for maintaining genome stability. Here, we report that SDE2, a PCNA-associated protein, plays a key role in maintaining active replication and counteracting replication stress by regulating the replication fork protection complex (FPC). SDE2 directly interacts with the FPC component TIMELESS (TIM) and enhances its stability, thereby aiding TIM localization to replication forks and the coordination of replisome progression. Like TIM deficiency, knockdown of SDE2 leads to impaired fork progression and stalled fork recovery, along with a failure to activate CHK1 phosphorylation. Moreover, loss of SDE2 or TIM results in an excessive MRE11-dependent degradation of reversed forks. Together, our study uncovers an essential role for SDE2 in maintaining genomic integrity by stabilizing the FPC and describes a new role for TIM in protecting stalled replication forks. We propose that TIM-mediated fork protection may represent a way to cooperate with BRCA-dependent fork stabilization. The fork protection complex (FPC), including the proteins TIMELESS and TIPIN, stabilizes the replisome to ensure unperturbed fork progression during DNA replication. Here the authors reveal that that SDE2, a PCNA-associated protein, plays an important role in maintaining active replication and protecting stalled forks by regulating the replication fork protection complex (FPC). -
dc.identifier.bibliographicCitation NATURE COMMUNICATIONS, v.11, no.1, pp.5495 -
dc.identifier.doi 10.1038/s41467-020-19162-5 -
dc.identifier.issn 2041-1723 -
dc.identifier.scopusid 2-s2.0-85094635515 -
dc.identifier.uri https://scholarworks.unist.ac.kr/handle/201301/49721 -
dc.identifier.url https://www.nature.com/articles/s41467-020-19162-5 -
dc.identifier.wosid 000588063600018 -
dc.language 영어 -
dc.publisher NATURE RESEARCH -
dc.title SDE2 integrates into the TIMELESS-TIPIN complex to protect stalled replication forks -
dc.type Article -
dc.description.isOpenAccess TRUE -
dc.relation.journalWebOfScienceCategory Multidisciplinary Sciences -
dc.relation.journalResearchArea Science & Technology - Other Topics -
dc.type.docType Article -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.subject.keywordPlus DNA-REPLICATION -
dc.subject.keywordPlus HOMOLOGOUS RECOMBINATION -
dc.subject.keywordPlus MRE11-DEPENDENT DEGRADATION -
dc.subject.keywordPlus GENOME STABILITY -
dc.subject.keywordPlus S-PHASE -
dc.subject.keywordPlus CHECKPOINT -
dc.subject.keywordPlus ATR -
dc.subject.keywordPlus REVERSAL -
dc.subject.keywordPlus STRESS -
dc.subject.keywordPlus DISTINCT -

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