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J. Exp. Med.,
Volume 187, Number 11, June 1, 1998 1735-1743
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From the * Basel Institute for Immunology, CH-4005 Basel, Switzerland; the To investigate the possible involvement of DNA repair in the process of somatic hypermutation of rearranged immunoglobulin variable (V) region genes, we have analyzed the occurrence, frequency, distribution, and pattern of mutations in rearranged V
Institute for Genetics,
University of Cologne, 50931 Cologne, Germany; the § Department of Cellular Biology and Genetics,
Erasmus University, 3000 DR Rotterdam, The Netherlands; the
Department of Molecular
Carcinogenesis, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; the ¶ Department of Immunology, University Hospital Utrecht, 3508 GA Utrecht, The Netherlands; the ** Ecole Superieure de Biotechnologie de Strasbourg, Université Louis Pasteur, F-67400
Illkirch-Graffenstaden, France; and the 
Department of Molecular and Cellular Toxicology,
Harvard School of Public Health, Boston, Massachusetts 02115
1 light chain genes
from naive and memory B cells in DNA repair-deficient mutant mouse strains. Hypermutation
was found unaffected in mice carrying mutations in either of the following DNA repair genes: xeroderma pigmentosum complementation group (XP)A and XPD, Cockayne syndrome complementation group B (CSB), mutS homologue 2 (MSH2), radiation sensitivity 54 (RAD54),
poly (ADP-ribose) polymerase (PARP), and 3-alkyladenine DNA-glycosylase (AAG). These
results indicate that both subpathways of nucleotide excision repair, global genome repair, and
transcription-coupled repair are not required for somatic hypermutation. This appears also to
be true for mismatch repair, RAD54-dependent double-strand-break repair, and AAG-mediated base excision repair.
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