@article{aa5442ed259a43bc87068d126e115989,
title = "Corepression of ReIA and c-Rel inhibits immunoglobulin κ gene transcription and rearrangement in precursor B lymphocytes",
abstract = "Multiple members of the NF-κB/Rel protein family are induced during B cell differentiation and have been implicated in transcriptional activation of the immunoglobulin κ (Igκ) locus. Despite these findings, normal numbers of Igκ+ B lymphocytes are produced by mice bearing targeted mutations in individual NF-κB/Rel genes. In the present study, precursor B lymphocytes were engineered to express a trans-dominant form of IκBα that simultaneously impairs the c-Rel and RelA transactivating subunits of NF-κB. This dual block in NF-κB/Rel signaling led to potent inhibition of germline Igκ transcription and rearrangement, whereas recombinase activity was unaffected. These findings suggest that c-Rel and RelA serve compensatory functional roles in the developmental mechanisms that govern Igκ gene assembly.",
author = "Scherer, {David C.} and Brockman, {Jeffrey A.} and Bendall, {Heather H.} and Zhang, {Guo Ming} and Ballard, {Dean W.} and Oltz, {Eugene M.}",
note = "Funding Information: Correspondence should be addressed to D. W. B. and E. M. O. We thank B. Van Ness, N. Rosenberg, S. Ghosh, and I. Verma for reagents; L. Van Kaer, M. Boothby, G. Hicks, M. Sikes, and B. Van Ness for critical comments on the manuscript; and E. Vance for manuscript preparation. This work was supported by the Howard Hughes Medical Institute, the National Institutes of Health (grants AI33839, AI36944, and AI01412), and the National Cancer Institute (CA09592). E. M. O. is a scholar of the Joe C. Davis Foundation and D. W. B. is an Investigator of the Howard Hughes Medical Institute.",
year = "1996",
month = dec,
doi = "10.1016/S1074-7613(00)80271-X",
language = "English",
volume = "5",
pages = "563--574",
journal = "Immunity",
issn = "1074-7613",
number = "6",
}