Transcription profiling of mouse lymph node derived B cells from Traf2 and Traf3 B cell knockout mice and Baff tg mice

ABSTRACT: Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-κB2 (NF-κB2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and

ORGANISM(S): Mus musculus

SUBMITTER: Sandra Gardam 

PROVIDER: E-GEOD-10422 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress