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PU.1/Spi-B regulation of c-rel is essential for mature B cell survival. Immunity 2001 Oct;15(4):545-55

Date

10/24/2001

Pubmed ID

11672537

DOI

10.1016/s1074-7613(01)00219-9

Scopus ID

2-s2.0-0034748923 (requires institutional sign-in at Scopus site)   42 Citations

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-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 MC

Author

Sridhar Rao MD, PhD Associate Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
B-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