A switch in distinct IκBα degradation mechanisms mediates constitutive NF-κB activation in mature B cells

Erika R. Fields, Bradley J. Seufzer, Eugene M. Oltz, Shigeki Miyamoto

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

Inducible activation of cytoplasmic NF-κB/Rel transcription factors occurs via proteasome-dependent degradation of an associated inhibitor, termed IκBa. Mature B lymphocytes constitutively express nuclear NF-κB, which is important for their long-term survival. The intrinsic mechanisms by which B cells constitutively activate NF-κB are unknown. In this paper we demonstrate that maintenance of NF-κB activity in primary B cells is mediated by a novel calcium-dependent, but proteasome-independent, mechanism. Moreover, we show that differentiation of conditionally transformed pre-B cells is accompanied by a switch from proteasome-dependent to proteasome- independent degradation of IκBα. Our findings indicate that IκBα degradation mechanisms are dynamic during B cell development, and ultimately establish constitutive NF-κB activity in mature B lymphocytes.

Original languageEnglish
Pages (from-to)4762-4767
Number of pages6
JournalJournal of Immunology
Volume164
Issue number9
StatePublished - May 1 2000

Fingerprint Dive into the research topics of 'A switch in distinct IκBα degradation mechanisms mediates constitutive NF-κB activation in mature B cells'. Together they form a unique fingerprint.

  • Cite this

    Fields, E. R., Seufzer, B. J., Oltz, E. M., & Miyamoto, S. (2000). A switch in distinct IκBα degradation mechanisms mediates constitutive NF-κB activation in mature B cells. Journal of Immunology, 164(9), 4762-4767.