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Arakawa, H. ; Buerstedde, J.-M.

Activation-induced cytidine deaminase-mediated hypermutation in the DT40 cell line.

Philos. Trans. R. Soc. B - Biol. Sci. 364(517), 639-644 (2008)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Depending on the species and the developmental stage of B cells, activation-induced cytidine deaminase (AID) triggers immunoglobulin (Ig) gene diversification by gene conversion, hypermutation or switch recombination. The bursal B cell line DT40 usually diversifies its rearranged Ig light chain (IgL) gene by gene conversion, but disruption of the RAD51 gene paralogues or deletion of the psiV conversion donors induces hypermutation. Although not all aspects of somatic hypermutation can be studied in DT40, the compact size of the chicken IgL locus and the ability to modify the genome by targeted integration are powerful experimental advantages. We review here how the studies in DT40 contributed to understanding how AID initiates Ig gene diversification and how AID-induced uracils are subsequently processed by uracil DNA glycosylase, proliferating cell nuclear antigens and error-prone polymerases. We also discuss the on-going research on the Ig locus specificity of hypermutation and the possibility of using hypermutation for the artificial evolution of proteins and regulatory sequences in DT40.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter activation-induced cytidine deaminase; DT40; gene conversion; immunoglobulin; somatic hypermutation
Sprache englisch
Veröffentlichungsjahr 2008
HGF-Berichtsjahr 2008
ISSN (print) / ISBN 0962-8436
e-ISSN 1471-2970
Zeitschrift Philosophical Transactions of the Royal Society of London. Series B
Quellenangaben Band: 364(517), Heft: 1517, Seiten: 639-644 Artikelnummer: , Supplement: ,
Verlag Royal Society of London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Radiation Biology (IMS)
PSP-Element(e) G-500400-001
DOI 10.1098/rstb.2008.0202
Scopus ID 60049095326
Erfassungsdatum 2008-12-31
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