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Significance Uniquely in B cells, deletion of the adaptor protein TRAF3 (TNF receptor-associated factor 3) causes enhanced survival; TRAF3 deficiency is observed in a substantial percentage of human B-cell malignancies. Here, we report that TRAF3 is a resident nuclear protein in B cells that regulates stability of the CREB (cAMP response element binding protein) transcription factor. This regulation is important for restraining B-cell survival by preventing transcription of prosurvival genes and may be a key mechanism by which loss of TRAF3 contributes to B-cell malignancies. Considering the high frequency ofTRAF3 mutations in B-cell tumors, our findings of an important nuclear role for TRAF3 present a new paradigm in understanding both normal regulation of B-cell survival and pathogenesis of B-cell cancers.

Nuclear TRAF3 is a negative regulator of CREB in B cells