ArticleCell cycle (Georgetown, Tex.)2020
SET8 localization to chromatin flanking DNA damage is dependent on RNF168 ubiquitin ligase.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin.Nature communications · 2024Article
- Roles for the methyltransferase SETD8 in DNA damage repair.Clinical epigenetics · 2022Review
- Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8.Cell cycle (Georgetown, Tex.)Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
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Abstract
The DNA damage response (DDR) associated post-translational modifications recruit chromatin remodelers, signaling proteins such as 53BP1 and repair factors to chromatin flanking DNA double strand breaks (DSBs) to promote its repair. Although localization of both RNF168 ubiquitin ligase and SET8 methyltransferase at DSBs is essential for 53BP1's recruitment to DSBs, it is unclear if they do so via the same pathways. Here we report that RNF168 mediates SET8's recruitment to DSBs. Depletion of cellular pool of ubiquitin through proteasome inhibition abolished RNF168 and SET8's localization to DNA damage. Knockdown of RNF8 or RNF168 abolished SET8's recruitment to DNA damage. Moreover, RNF168 and SET8 form stable complexes
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