Academic Journal

RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair

التفاصيل البيبلوغرافية
العنوان: RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair
المؤلفون: Katsuki, Yoko, Abe, Masako, Park, Seon Young, Wu, Wenwen, Yabe, Hiromasa, Yabe, Miharu, van Attikum, Haico, Nakada, Shinichiro, Ohta, Tomohiko, Seidman, Michael M., Kim, Yonghwan, Takata, Minoru
المساهمون: 勝木, 陽子, 安倍, 昌子, 矢部, 普正, 矢部, みはる, 中田, 慎一郎, 太田, 智彦, 髙田, 穣, 30281728
بيانات النشر: Elsevier BV
سنة النشر: 2021
المجموعة: Kyoto University Research Information Repository (KURENAI) / 京都大学学術情報リポジトリ
مصطلحات موضوعية: Fanconi anemia, interstrand crosslink repair, SLX4, ubiquitination, RNF168
الوصف: 遺伝性血液疾患の原因タンパク質を制御する新規のユビキチン経路を解明 --ファンコニ貧血にかかわる新たな関連因子群の同定--. 京都大学プレスリリース. 2021-10-28. ; SLX4/FANCP is a key Fanconi anemia (FA) protein and a DNA repair scaffold for incision around a DNA interstrand crosslink (ICL) by its partner XPF nuclease. The tandem UBZ4 ubiquitin-binding domains of SLX4 are critical for the recruitment of SLX4 to damage sites, likely by binding to K63-linked polyubiquitin chains. However, the identity of the ubiquitin E3 ligase that mediates SLX4 recruitment remains unknown. Using small interfering RNA (siRNA) screening with a GFP-tagged N-terminal half of SLX4 (termed SLX4-N), we identify the RNF168 E3 ligase as a critical factor for mitomycin C (MMC)-induced SLX4 foci formation. RNF168 and GFP-SLX4-N colocalize in MMC-induced ubiquitin foci. Accumulation of SLX4-N at psoralen-laser ICL tracks or of endogenous SLX4 at Digoxigenin-psoralen/UVA ICL is dependent on RNF168. Finally, we find that RNF168 is epistatic with SLX4 in promoting MMC tolerance. We conclude that RNF168 is a critical component of the signal transduction that recruits SLX4 to ICL damage.
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 34706224
2211-1247
Relation: https://www.kyoto-u.ac.jp/ja/research-news/2021-10-28-0; http://hdl.handle.net/2433/265791; Cell Reports; 37; 109879
الاتاحة: http://hdl.handle.net/2433/265791
Rights: © 2021 The Author(s). ; This is an open access article under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International license. ; http://creativecommons.org/licenses/by-nc-nd/4.0/
رقم الانضمام: edsbas.9D1CB77D
قاعدة البيانات: BASE