A critical role of TAK1 in B-cell receptor-mediated nuclear factor kappaB activation. Blood 2009 May 07;113(19):4566-74
Date
02/07/2009Pubmed ID
19196865Pubmed Central ID
PMC2680363DOI
10.1182/blood-2008-08-176057Scopus ID
2-s2.0-66549125216 (requires institutional sign-in at Scopus site) 71 CitationsAbstract
The kinase TAK1 is essential for T-cell receptor (TCR)-mediated nuclear factor kappaB (NF-kappaB) activation and T-cell development. However, the role of TAK1 in B-cell receptor (BCR)-mediated NF-kappaB activation and B-cell development is not clear. Here we show that B-cell-specific deletion of TAK1 impaired the transition from transitional type 2 to mature follicular (FO) B cells and caused a marked decrease of marginal zone (MZ) B cells. TAK1-deficient B cells exhibited an increase of BCR-induced apoptosis and impaired proliferation in response to BCR ligation. Importantly, TAK1-deficient B cells failed to activate NF-kappaB after BCR stimulation. Thus, TAK1 is critical for B-cell maturation and BCR-induced NF-kappaB activation.
Author List
Schuman J, Chen Y, Podd A, Yu M, Liu HH, Wen R, Chen ZJ, Wang DMESH terms used to index this publication - Major topics in bold
AnimalsApoptosis
B-Lymphocytes
Blotting, Western
Cell Nucleus
Electrophoretic Mobility Shift Assay
Flow Cytometry
Fluorescent Antibody Technique
MAP Kinase Kinase Kinases
Mice
Mice, Knockout
NF-kappa B
Receptors, Antigen, B-Cell
Signal Transduction
