Faculty Collaboration Database

A critical role of TAK1 in B-cell receptor-mediated nuclear factor kappaB activation. Blood 2009 May 07;113(19):4566-74

Date

02/07/2009

Pubmed ID

19196865

Pubmed Central ID

PMC2680363

DOI

10.1182/blood-2008-08-176057

Scopus ID

2-s2.0-66549125216 (requires institutional sign-in at Scopus site)   69 Citations

Abstract

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 D

Authors

Demin Wang PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin
Renren Wen PhD Adjunct Associate Professor in the Microbiology and Immunology department at Medical College of Wisconsin

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

Animals
Apoptosis
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