REFERENCES
- Arenzana-Seisdedos, F., P. Turpin, M. Rodriguez, D. Thomas, R. T. Hay, J. L. Virelizier, and C. Dargemont. 1997. Nuclear localization of IκBα promotes active transport of NF-κB from the nucleus to the cytoplasm. J. Cell Sci. 110:369–378.
- Bajpai, U. D., K. Zhang, M. Teutsch, R. Sen, and H. H. Wortis. 2000. Bruton's tyrosine kinase links the B cell receptor to nuclear factor κB activation. J. Exp. Med. 191:1735–1744.
- Beg, A. A., W. C. Sha, R. T. Bronson, and D. Baltimore. 1995. Constitutive NF-κB activation, enhanced granulopoiesis, and neonatal lethality in Iκ Bα-deficient mice. Genes Dev. 9:2736–2746.
- Blank, V., P. Kourilsky, and A. Israel. 1991. Cytoplasmic retention, DNA binding and processing of the NF-κB p50 precursor are controlled by a small region in its C-terminus. EMBO J. 10:4159–4167.
- Cramer, P., and C. W. Muller. 1999. A firm hand on NFκB: structures of the IκBα-NFκB complex. Structure Fold Des. 7:R1–R6.
- Doerre, S., and R. B. Corley. 1999. Constitutive nuclear translocation of NF-κB in B cells in the absence of IκB degradation. J. Immunol. 163:269–277.
- Ellmeier, W., S. Jung, M. J. Sunshine, F. Hatam, Y. Xu, D. Baltimore, H. Mano, and D. R. Littman. 2000. Severe B cell deficiency in mice lacking the Tec kinase family members Tec and Btk. J. Exp. Med. 192:1611–1624.
- Feske, S., R. Draeger, H. H. Peter, K. Eichmann, and A. Rao. 2000. The duration of nuclear residence of NFAT determines the pattern of cytokine expression in human SCID T cells. J. Immunol. 165:297–305.
- Fields, E. R., B. J. Seufzer, E. M. Oltz, and S. Miyamoto. 2000. A switch in distinct IκBα degradation mechanisms mediates constitutive NF-κB activation in mature B cells. J. Immunol. 164:4762–4767.
- Gerondakis, S., A. Strasser, D. Metcalf, G. Grigoriadis, J. Y. Scheerlinck, and R. J. Grumont. 1996. Rel-deficient T cells exhibit defects in production of interleukin 3 and granulocyte-macrophage colony-stimulating factor. Proc. Natl. Acad. Sci. USA 93:3405–3409.
- Grossmann, M., Y. Nakamura, R. Grumont, and S. Gerondakis. 1999. New insights into the roles of Rel/NFκB transcription factors in immune function, hemopoiesis and human disease. Int. J. Biochem. Cell Biol. 31:1209–1219.
- Grossmann, M., L. A. O'Reilly, R. Gugasyan, A. Strasser, J. M. Adams, and S. Gerondakis. 2000. The anti-apoptotic activities of Rel and RelA required during B-cell maturation involve the regulation of Bcl-2 expression. EMBO J. 19:6351–6360.
- Grumont, R. J., and S. Gerondakis. 1994. The subunit composition of NF-κB complexes changes during B-cell development. Cell Growth Differ. 5:1321–1331.
- Harhaj, E. W., and S. C. Sun. 1999. Regulation of RelA subcellular localization by a putative nuclear export signal and p50. Mol. Cell. Biol. 19:7088–7095.
- Hay, R. T., L. Vuillard, J. M. Desterro, and M. S. Rodriguez. 1999. Control of NF-κB transcriptional activation by signal induced proteolysis of IκBα. Phil. Trans. R. Soc. Lond. B Biol. Sci. 354:1601–1609.
- Huang, T. T., N. Kudo, M. Yoshida, and S. Miyamoto. 2000. A nuclear export signal in the N-terminal regulatory domain of IκBα controls cytoplasmic localization of inactive NF-κB/IκBα complexes. Proc. Natl. Acad. Sci. USA 97:1014–1019.
- Huxford, T., D. B. Huang, S. Malek, and G. Ghosh. 1998. The crystal structure of the IκBα/NF-κB complex reveals mechanisms of NF-κB inactivation. Cell 95:759–770.
- Jacobs, M. D., and S. C. Harrison. 1998. Structure of an IκBα/NF-κB complex. Cell 95:749–758.
- Johnson, C., D. Van Antwerp, and T. J. Hope. 1999. An N-terminal nuclear export signal is required for the nucleocytoplasmic shuttling of IκBα. EMBO J. 18:6682–6693.
- Kerner, J. D., M. W. Appleby, R. N. Mohr, S. Chien, D. J. Rawlings, C. R. Maliszewski, O. N. Witte, and R. M. Perlmutter. 1995. Impaired expansion of mouse B cell progenitors lacking Btk. Immunity 3:301–312.
- Khan, W. N., F. W. Alt, R. M. Gerstein, B. A. Malynn, I. Larsson, G. Rathbun, L. Davidson, S. Muller, A. B. Kantor, L. A. Herzenberg, et al.. 1995. Defective B cell development and function in Btk-deficient mice. Immunity 3:283–299.
- Kistler, B., A. Rolink, R. Marienfeld, M. Neumann, and T. Wirth. 1998. Induction of nuclear factor-κB during primary B cell differentiation. J. Immunol. 160:2308–2317.
- Klaus, G. G., M. Holman, C. Johnson-Leger, C. Elgueta-Karstegl, and C. Atkins. 1997. A re-evaluation of the effects of X-linked immunodeficiency (xid) mutation on B cell differentiation and function in the mouse. Eur. J. Immunol. 27:2749–2756.
- Klement, J. F., N. R. Rice, B. D. Car, S. J. Abbondanzo, G. D. Powers, P. H. Bhatt, C. H. Chen, C. A. Rosen, and C. L. Stewart. 1996. IκBα deficiency results in a sustained NF-κB response and severe widespread dermatitis in mice. Mol. Cell. Biol. 16:2341–2349.
- Krappmann, D., and C. Scheidereit. 1997. Regulation of NF-κB activity by IκBα and IκBβ stability. Immunobiology 198:3–13.
- Liou, H. C., Z. Jin, J. Tumang, S. Andjelic, K. A. Smith, and M. L. Liou. 1999. c-Rel is crucial for lymphocyte proliferation but dispensable for T cell effector function. Int. Immunol. 11:361–371.
- Liou, H. C., W. C. Sha, M. L. Scott, and D. Baltimore. 1994. Sequential induction of NF-κB/Rel family proteins during B-cell terminal differentiation. Mol. Cell. Biol. 14:5349–5359.
- May, M. J., and S. Ghosh. 1997. Rel/NF-κB and IκB proteins: an overview. Semin. Cancer Biol. 8:63–73.
- Miyamoto, S., P. J. Chiao, and I. M. Verma. 1994. Enhanced IκBα degradation is responsible for constitutive NF-κB activity in mature murine B-cell lines. Mol. Cell. Biol. 14:3276–3282.
- Miyamoto, S., M. J. Schmitt, and I. M. Verma. 1994. Qualitative changes in the subunit composition of κB-binding complexes during murine B-cell differentiation. Proc. Natl. Acad. Sci. USA 91:5056–5060.
- Miyamoto, S., B. J. Seufzer, and S. D. Shumway. 1998. Novel IκBα proteolytic pathway in WEHI231 immature B cells. Mol. Cell. Biol. 18:19–29.
- Nelsen, B., G. Tian, B. Erman, J. Gregoire, R. Maki, B. Graves, and R. Sen. 1993. Regulation of lymphoid-specific immunoglobulin μ heavy chain gene enhancer by ETS-domain proteins. Science 261:82–86.
- Ossareh-Nazari, B., F. Bachelerie, and C. Dargemont. 1997. Evidence for a role of CRM1 in signal-mediated nuclear protein export. Science 278:141–144.
- Pahl, H. L.. 1999. Activators and target genes of Rel/NF-κB transcription factors. Oncogene 18:6853–6866.
- Phelps, C. B., L. L. Sengchanthalangsy, T. Huxford, and G. Ghosh. 2000. Mechanism of IκBα binding to NF-κB dimers. J. Biol. Chem. 275:29840–29846.
- Phillips, R. J., and S. Ghosh. 1997. Regulation of IκBβ in WEHI 231 mature B cells. Mol. Cell. Biol. 17:4390–4396.
- Prigent, M., I. Barlat, H. Langen, and C. Dargemont. 2000. IκBα and IκBα/NF-κB complexes are retained in the cytoplasm through interaction with a novel partner, RasGAP SH3-binding protein 2. J. Biol. Chem. 275:36441–36449.
- Satterthwaite, A. B., Z. Li, and O. N. Witte. 1998. Btk function in B cell development and response. Semin. Immunol. 10:309–316.
- Sha, W. C., H. C. Liou, E. I. Tuomanen, and D. Baltimore. 1995. Targeted disruption of the p50 subunit of NF-κB leads to multifocal defects in immune responses. Cell 80:321–330.
- Shumway, S. D., M. Maki, and S. Miyamoto. 1999. The PEST domain of IκBα is necessary and sufficient for in vitro degradation by μ-calpain. J. Biol. Chem. 274:30874–30881.
- Snapper, C. M., P. Zelazowski, F. R. Rosas, M. R. Kehry, M. Tian, D. Baltimore, and W. C. Sha. 1996. B cells from p50/NF-κB knockout mice have selective defects in proliferation, differentiation, germ-line CH transcription, and Ig class switching. J. Immunol. 156:183–191.
- Tam, W. F., L. H. Lee, L. Davis, and R. Sen. 2000. Cytoplasmic sequestration of Rel proteins by IκBα requires CRM1-dependent nuclear export. Mol. Cell. Biol. 20:2269–2284.
- Tam, W. F., and R. Sen. 2001. IκB family member function by different mechanisms. J. Biol. Chem. 276:7701–7704.
- Whiteside, S. T., and A. Israel. 1997. IκB proteins: structure, function and regulation. Semin. Cancer Biol. 8:75–82.
- Zabel, U., T. Henkel, M. S. Silva, and P. A. Baeuerle. 1993. Nuclear uptake control of NF-κB by MAD-3, an IκB protein present in the nucleus. EMBO J. 12:201–211.