Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.

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作者： Michael X,Le ^[1] ; Dania,Haddad ^[1] ; Alexanda K,Ling ^[1] ; Conglei,Li ^[1] ; Clare C,So ^[1] ; Amit,Chopra ^[1] ; Rui,Hu ^[1] ; Jaime F,Angulo ^[2] ; Jason,Moffat ^[3] ; Alberto,Martin ^[1]

作者单位： Department of Immunology, University of Toronto, Medical Sciences Building, Toronto, Ontario, M5S1A8, Canada. ^[1] Laboratoire de Radio Toxicologie, CEA, Université Paris-Saclay, Arpajon, 91297, France. ^[2] Donnelly Centre and Banting and Best Department of Medical Research, University of Toronto, Toronto, Ontario, M5S1A8, Canada. ^[3]

主题词 B-淋巴细胞(B-Lymphocytes);细胞系, 肿瘤(Cell Line, Tumor);DNA断裂, 双链(DNA Breaks, Double-Stranded);DNA结合蛋白质类(DNA-Binding Proteins);人类(Humans);免疫球蛋白类别转换(Immunoglobulin Class Switching);RNA结合蛋白质类(RNA-Binding Proteins)

DOI 10.1038/srep37215

PMID 27853268

发布时间 2024-06-03

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Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.

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Kin17 facilitates multiple double-strand break repair pathways that govern B cell class switching.

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