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Cutting Edge: TFII-I Controls B Cell Proliferation via Regulating NF-B¹

Todd Ashworth^* and Ananda L. Roy^2,*,,

^* Program in Immmunology and Program in Genetics, Department of Pathology, Tufts University School of Medicine, Boston, MA 02111

The multifunctional transcription factor TFII-I physically and functionally interacts with Bruton’s tyrosine kinase in murine B cells. However, the downstream functions of TFII-I in B cells are unknown. Toward achieving this goal, we established stable posttranscriptional silencing of TFII-I in WEHI-231 immature murine B cells, which undergoes growth arrest and apoptosis either upon anti-IgM or TGF- signaling. In this study, we show that TFII-I promotes growth arrest of cells in a signal-dependent manner. Unlike control cells, B cells exhibiting loss of TFII-I function fail to undergo arrest upon signaling due to up-regulation of c-Myc expression and concomitant down-regulation of both p21 and p27. Loss of TFII-I is also associated with simultaneous increase in nuclear c-rel and decrease in p50 homodimer binding. Thus, besides controlling c-myc transcription, TFII-I controls B cell proliferation by regulating both nuclear translocation of c-rel and DNA-binding activity of p50 NF-B.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by a grant from National Institutes of Health (AI 45150; to A.L.R.).

² Address correspondence and reprint requests to Dr. Ananda L. Roy, Department of Pathology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111. E-mail address: ananda.roy{at}tufts.edu

³ Abbreviations used in this paper: Bcr, B cell Ag receptor; Btk, Bruton’s tyrosine kinase; sh, short hairpin; KD, knockdown.

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