دورية أكاديمية
أعرض في EDS

RNAi Screening Uncovers a Synthetic Sick Interaction between CtIP and the BARD1 Tumor Suppressor.

التفاصيل البيبلوغرافية
العنوان: RNAi Screening Uncovers a Synthetic Sick Interaction between CtIP and the BARD1 Tumor Suppressor.
المؤلفون: Bolck HA; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.; Institute of Pathology and Molecular Pathology, University Hospital Zurich, 8091 Zurich, Switzerland., Przetocka S; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.; Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA., Meier R; Scientific Center for Optical and Electron Microscopy (ScopeM), ETH Zurich, 8093 Zurich, Switzerland., von Aesch C; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland., Zurfluh C; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland., Hänggi K; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.; Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA., Spegg V; Department of Molecular Mechanisms of Disease, University of Zurich, 8057 Zurich, Switzerland., Altmeyer M; Department of Molecular Mechanisms of Disease, University of Zurich, 8057 Zurich, Switzerland., Stebler M; Scientific Center for Optical and Electron Microscopy (ScopeM), ETH Zurich, 8093 Zurich, Switzerland., Nørrelykke SF; Scientific Center for Optical and Electron Microscopy (ScopeM), ETH Zurich, 8093 Zurich, Switzerland., Horvath P; Synthetic and System Biology Unit, Biological Research Center (BRC), 6726 Szeged, Hungary.; Institute for Molecular Medicine Finland, University of Helsinki, 00014 Helsinki, Finland., Sartori AA; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland., Porro A; Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.
المصدر: Cells [Cells] 2022 Feb 12; Vol. 11 (4). Date of Electronic Publication: 2022 Feb 12.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: DNA Breaks, Double-Stranded* , DNA Repair* , Endodeoxyribonucleases*/genetics , Endodeoxyribonucleases*/metabolism , Tumor Suppressor Proteins*/genetics , Tumor Suppressor Proteins*/metabolism , Ubiquitin-Protein Ligases*/genetics , Ubiquitin-Protein Ligases*/metabolism, Genes, Tumor Suppressor ; Homologous Recombination ; Humans ; RNA Interference
مستخلص: Human CtIP is best known for its role in DNA end resection to initiate DNA double-strand break repair by homologous recombination. Recently, CtIP has also been shown to protect reversed replication forks from nucleolytic degradation upon DNA replication stress. However, still little is known about the DNA damage response (DDR) networks that preserve genome integrity and sustain cell survival in the context of CtIP insufficiency. Here, to reveal such potential buffering relationships, we screened a DDR siRNA library in CtIP-deficient cells to identify candidate genes that induce synthetic sickness/lethality (SSL). Our analyses unveil a negative genetic interaction between CtIP and BARD1, the heterodimeric binding partner of BRCA1. We found that simultaneous disruption of CtIP and BARD1 triggers enhanced apoptosis due to persistent replication stress-induced DNA lesions giving rise to chromosomal abnormalities. Moreover, we observed that the genetic interaction between CtIP and BARD1 occurs independently of the BRCA1-BARD1 complex formation and might be, therefore, therapeutical relevant for the treatment of BRCA-defective tumors.
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معلومات مُعتمدة: PP00P3_179057 Switzerland SNSF_ Swiss National Science Foundation; 310030_197003 Switzerland SNSF_ Swiss National Science Foundation; 31003A_176161 Switzerland SNSF_ Swiss National Science Foundation; United Kingdom WT_ Wellcome Trust; 31003A_156023 Switzerland SNSF_ Swiss National Science Foundation; ERC-2016-STG 714326 International ERC_ European Research Council
فهرسة مساهمة: Keywords: BARD1; BRCA1; CtIP; DNA damage; replication stress; synthetic lethality
المشرفين على المادة: 0 (Tumor Suppressor Proteins)
EC 2.3.2.27 (BARD1 protein, human)
EC 2.3.2.27 (Ubiquitin-Protein Ligases)
EC 3.1.- (Endodeoxyribonucleases)
EC 3.1.- (RBBP8 protein, human)
تواريخ الأحداث: Date Created: 20220225 Date Completed: 20220408 Latest Revision: 20240511
رمز التحديث: 20240511
مُعرف محوري في PubMed: PMC8870135
DOI: 10.3390/cells11040643
PMID: 35203293
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells11040643