The DOI matches its Crossref record; 101 of the 101 references it cites were found in a registry or an index.
Mechanisms of Programmed DNA Lesions and Genomic Instability in the Immune System
Open accessAbstract
Chromosomal translocations involving antigen receptor loci are common in lymphoid malignancies. Translocations require DNA double-strand breaks (DSBs) at two chromosomal sites, their physical juxtaposition, and their fusion by end joining. Ability of lymphocytes to generate diverse repertoires of antigen receptors and effector antibodies derives from programmed genomic alterations that produce DSBs. We discuss these lymphocyte-specific processes, with a focus on mechanisms that provide requisite DSB target specificity and mechanisms that suppress DSB translocation. We also discuss recent work that provides new insights into DSB repair pathways and influences of three-dimensional genome organization on physiological processes and cancer genomes.
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Cites
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Cited by
Formation of chromosomal domains by loop extrusion
Fudenberg, G., Imakaev, M., Lu, C., Goloborodko, A., Abdennur, N., & Mirny, L. A. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.04.085 · Cited by 2,003
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CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function
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Genome-wide detection of DNA double-stranded breaks induced by engineered nucleases
Frock, R. L., Hu, J., Meyers, R. M., Ho, Y.-J., Kii, E., & Alt, F. W. (2015) · Nature Biotechnology · doi:10.1038/nbt.3101 · Cited by 673
Base excision repair: A critical player in many games
Wallace, S. S. (2014) · DNA Repair · doi:10.1016/j.dnarep.2014.03.030 · Cited by 401
Metadata
- Authors
- Alt, F. W., Zhang, Y., Meng, F.-L., Guo, C., & Schwer, B.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-01
- Volume
- 152
- Issue
- 3
- Pages
- 417-429
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2139891717
- Cited by
- 484
- References
- 101
- FWCI
- 22.19
- Type
- journal article
- Language
- en
- Open access
- bronze
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