Abstract：
:One of the most toxic insults a cell can incur is a disruption of its linear DNA in the form of a double-strand break (DSB). Left unrepaired, or repaired improperly, these lesions can result in cell death or neoplastic transformation. Despite these dangers, lymphoid cells purposely introduce DSBs into their genome to maximize the diversity and effector functions of their antigen receptor genes. While the generation of breaks requires distinct lymphoid-specific factors, their resolution requires various ubiquitously expressed DNA-repair proteins, known collectively as the non-homologous end-joining pathway. In this review, we discuss the factors that constitute this pathway as well as the evidence of their involvement in two lymphoid-specific DNA recombination events.
journal_name
Immunol Revjournal_title
Immunological reviewsauthors
Rooney S,Chaudhuri J,Alt FWdoi
10.1111/j.0105-2896.2004.00165.xkeywords:
subject
Has Abstractpub_date
2004-08-01 00:00:00pages
115-31eissn
0105-2896issn
1600-065Xpii
IMR165journal_volume
200pub_type
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