PU.1/Spi-B regulation of c-rel is essential for mature B cell survival

Author(s): Hu, CJ; Rao, S; Ramirez-Bergeron, DL; Garrett-Sinha, LA; Gerondakis, S; Clark, MR; Simon, MC;
Details: Publication Year 2001-10,Volume 15,Issue #4,Page 545-555
Journal Title: IMMUNITY
Publication Type: Journal Article
Abstract: PU.1(+/-)Spi-B-/- mice exhibit reduced numbers of immature and mature B lymphocytes, which exhibit severe defects in response to BCR-mediated stimulation and poor survival. We found that expression of c-rel, a member of the Rel/NF-kappaB family, is dramatically reduced in PU.1(+/-)Spi-B-/- splenic B cells. Analysis of the murine c-rel promoter identified three PU.1/Spi-B binding sites critical for c-rel promoter activity. Furthermore, reintroduction of Rel protein restored wild-type B cell numbers to mice reconstituted with PU.1(+/-)Spi-B-/- bone marrow. These findings are the first to demonstrate that a member of the Rel/NF-kappaB family is directly regulated by Ets proteins and dissect the molecular basis for the function of two Ets factors, PU.1 and Spi-B, in promoting B lymphocyte survival.
Publisher: CELL PRESS
Keywords: NF-KAPPA-B; TRANSCRIPTION FACTOR PU.1; SPI-B; DNA-BINDING; LYMPHOCYTE DEVELOPMENT; NUCLEAR FACTOR; ETS-PROTEIN; T-CELL; SUBUNIT COMPOSITION; CYCLE PROGRESSION
Publisher's Version: https://doi.org/10.1016/S1074-7613(01)00219-9
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2001-10-01 12:00:00