RAG1/2 induces genomic insertions by mobilizing DNA into RAG1/2-independent breaks
نویسندگان
چکیده
منابع مشابه
RAG1/2 induces genomic insertions by mobilizing DNA into RAG1/2-independent breaks
The RAG recombinase (RAG1/2) plays an essential role in adaptive immunity by mediating V(D)J recombination in developing lymphocytes. In contrast, aberrant RAG1/2 activity promotes lymphocyte malignancies by causing chromosomal translocations and DNA deletions at cancer genes. RAG1/2 can also induce genomic DNA insertions by transposition and trans-V(D)J recombination, but only few such putativ...
متن کاملCorrection: RAG1/2 induces genomic insertions by mobilizing DNA into RAG1/2-independent breaks
The cancer datasets used in this study (dbGaP: phs000341.v2.p1 and phs000340.v3.p1; EBI: EGAS00001000399) were generated with the financial support of the National Cancer Institute, the St. Baldrick’s Foundation, Partners for Cures, the American Lebanese Syrian Associated Charities of St. Jude Children’s Research Hospital as part of the St. Jude/Washington University Pediatric Cancer Genome Pro...
متن کاملDNA Breaks Promote Genomic Instability by Impeding Proper Chromosome Segregation
BACKGROUND Unrepaired DNA double-stranded breaks (DSBs) can result in the whole or partial loss of chromosomes. Previously, we showed that the ends of broken chromosomes remain associated. Here, we have examined the machinery that holds broken chromosome ends together, and we have explored the behavior of broken chromosomes as they pass through mitosis. RESULTS Using GFP-localized arrays flan...
متن کاملDNA Double-Strand Breaks Come into Focus
The Mre11-Rad50-Nbs1 (MRN) complex senses DNA double-strand breaks and recruits different repair pathway and checkpoint proteins to break foci. Two new studies (Williams et al., 2009; Lloyd et al., 2009) identify Nbs1 as a key factor in this process and reveal how an N-terminal protein recruitment module in Nbs1 binds to different response factors through shared phosphopeptide motifs.
متن کاملThe role of DNA breaks in genomic instability and tumorigenesis.
DNA double-strand breaks (DSBs) represent dangerous chromosomal lesions that can lead to mutation, neoplastic transformation, or cell death. DSBs can occur by extrinsic insult from environmental sources or may occur intrinsically as a result of cellular metabolism or a genetic program. Mammalian cells possess potent and efficient mechanisms to repair DSBs, and thus complete normal development a...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Experimental Medicine
سال: 2017
ISSN: 0022-1007,1540-9538
DOI: 10.1084/jem.20161638