PU.1/Spi-B regulation of c-rel is essential for mature B cell survival. Immunity 2001 Oct;15(4):545-55
Date
10/24/2001Pubmed ID
11672537DOI
10.1016/s1074-7613(01)00219-9Scopus ID
2-s2.0-0034748923 (requires institutional sign-in at Scopus site) 42 CitationsAbstract
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-kappa B 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-kappa B 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.
Author List
Hu CJ, Rao S, Ramirez-Bergeron DL, Garrett-Sinha LA, Gerondakis S, Clark MR, Simon MCAuthor
Sridhar Rao MD, PhD Associate Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsB-Lymphocytes
Binding Sites
Bone Marrow Cells
Bone Marrow Transplantation
Cell Line
Cell Survival
Cells, Cultured
DNA-Binding Proteins
Down-Regulation
Gene Expression Regulation
Mice
Mice, Knockout
Promoter Regions, Genetic
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2
Proto-Oncogene Proteins c-rel
RNA, Messenger
Spleen
Trans-Activators
Transcription Factors
Transfection