دورية أكاديمية
أعرض في EDS

The role of SLFN11 in DNA replication stress response and its implications for the Fanconi anemia pathway.

التفاصيل البيبلوغرافية
العنوان: The role of SLFN11 in DNA replication stress response and its implications for the Fanconi anemia pathway.
المؤلفون: Mu A; Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Kyoto, Japan; Multilayer Network Research Unit, Research Coordination Alliance, Kyoto University, Kyoto, Japan. Electronic address: mu.anfeng.7x@kyoto-u.ac.jp., Okamoto Y; Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Kyoto, Japan; Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan., Katsuki Y; Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Kyoto, Japan., Takata M; Laboratory of DNA Damage Signaling, Department of Late Effects Studies, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Kyoto, Japan; Multilayer Network Research Unit, Research Coordination Alliance, Kyoto University, Kyoto, Japan. Electronic address: takata.minoru.8s@kyoto-u.ac.jp.
المصدر: DNA repair [DNA Repair (Amst)] 2024 Sep; Vol. 141, pp. 103733. Date of Electronic Publication: 2024 Jul 24.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101139138 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1568-7856 (Electronic) Linking ISSN: 15687856 NLM ISO Abbreviation: DNA Repair (Amst) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam ; New York : Elsevier, c2002-
مواضيع طبية MeSH: DNA Replication* , Fanconi Anemia*/metabolism , Fanconi Anemia*/genetics , DNA Damage* , Nuclear Proteins*/metabolism , Nuclear Proteins*/genetics, Humans ; Animals ; DNA Repair ; Fanconi Anemia Complementation Group Proteins/metabolism ; Fanconi Anemia Complementation Group Proteins/genetics
مستخلص: Fanconi anemia (FA) is a hereditary disorder characterized by a deficiency in the repair of DNA interstrand crosslinks and the response to replication stress. Endogenous DNA damage, most likely caused by aldehydes, severely affects hematopoietic stem cells in FA, resulting in progressive bone marrow failure and the development of leukemia. Recent studies revealed that expression levels of SLFN11 affect the replication stress response and are a strong determinant in cell killing by DNA-damaging cancer chemotherapy. Because SLFN11 is highly expressed in the hematopoietic system, we speculated that SLFN11 may have a significant role in FA pathophysiology. Indeed, we found that DNA damage sensitivity in FA cells is significantly mitigated by the loss of SLFN11 expression. Mechanistically, we demonstrated that SLFN11 destabilizes the nascent DNA strands upon replication fork stalling. In this review, we summarize our work regarding an interplay between SLFN11 and the FA pathway, and the role of SLFN11 in the response to replication stress.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Fanconi anemia; Hematopoiesis; RAD51; Replication stress; SLFN11
المشرفين على المادة: 0 (SLFN11 protein, human)
0 (Nuclear Proteins)
0 (Fanconi Anemia Complementation Group Proteins)
تواريخ الأحداث: Date Created: 20240803 Date Completed: 20240816 Latest Revision: 20240926
رمز التحديث: 20240926
DOI: 10.1016/j.dnarep.2024.103733
PMID: 39096698
قاعدة البيانات: MEDLINE
الوصف
تدمد:1568-7856
DOI:10.1016/j.dnarep.2024.103733