ArticleScientific reports2016
Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Roles and regulatory mechanisms of KIN17 in cancers (Review).Oncology letters · 2023Review
- A genetic screen in C. elegans reveals roles for KIN17 and PRCC in maintaining 5' splice site identity.PLoS genetics · 2022Article
- Interactome Analysis of KIN (Kin17) Shows New Functions of This Protein.Current issues in molecular biology · 2021Article
- KIN17 promotes tumor metastasis by activating EMT signaling in luminal-A breast cancer.Thoracic cancer · 2021Article
- Comparative Multiplexed Interactomics of SARS-CoV-2 and Homologous Coronavirus Nonstructural Proteins Identifies Unique and Shared Host-Cell Dependencies.ACS infectious diseases · 2020Article
- Comparative multiplexed interactomics of SARS-CoV-2 and homologous coronavirus non-structural proteins identifies unique and shared host-cell dependencies.bioRxiv : the preprint server for biology · 2020Article
- Biophysical characterization and molecular phylogeny of human KIN protein.European biophysics journal : EBJ · 2019Article
- Integrative genomic analysis identifies associations of molecular alterations to APOBEC and BRCA1/2 mutational signatures in breast cancer.Molecular genetics & genomic medicine · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Class switch recombination (CSR) in B cells requires the timely repair of DNA double-stranded breaks (DSBs) that result from lesions produced by activation-induced cytidine deaminase (AID). Through a genome-wide RNAi screen, we identified Kin17 as a gene potentially involved in the maintenance of CSR in murine B cells. In this study, we confirm a critical role for Kin17 in CSR independent of AID activity. Furthermore, we make evident that DSBs generated by AID or ionizing radiation require Kin17 for efficient repair and resolution. Our report shows that reduced Kin17 results in an elevated deletion frequency following AID mutational activity in the switch region. In addition, deficiency in Kin17 affects the functionality of multiple DSB repair pathways, namely homologous recombination, non-homologous end-joining, and alternative end-joining. This report demonstrates the importance of Kin17 as a critical factor that acts prior to the repair phase of DSB repair and is of bona fide importance for CSR.
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Registered trials
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