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. 2009 Aug 3;206(8):1803–1816. doi: 10.1084/jem.20082815

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© 2009 Cadera et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 5. — Cells undergoing receptor editing show increased IκBα levels as well as increased nuclear NF-κB and RPS3. (A) Bone marrow was isolated from IκBα^+/lacZ B1-8 α-HEL-κ, IκBα^+/lacZB1-8^high α-HEL-κ, and IκBα^+/lacZB1-8^low α-HEL-κ mice. Cells were loaded with FDG and stained with anti-CD19, anti-CD43, anti-IgM, and anti-IgD antibodies. Cells were first gated on IgD⁻. CD19 verses IgM staining is displayed. (B) β-gal activity in the CD19⁺IgD⁻ gate (pro–B, pre–B, and immature B cells) is displayed. IκBα^+/lacZ B1-8 α-HEL-κ is shaded gray, IκBα^+/lacZB1-8^low α-HEL-κ is the thin black line, and IκBα^+/lacZB1-8^high α-HEL-κ the thick black line. A and B are representative of at least three different mice individually analyzed for each genotype. (C) Immunofluorescence microscopy detecting p65 and RPS3 in B1-8 α-HEL-κ, B1-8^low α-HEL-κ, and B1-8^high α-HEL-κ pro–B, pre–B, and immature B cells. The data shown is representative of two independent sorts on each occasion scoring between 250 and 400 cells. Bar, 10 µm. Fig. S3 displays quantitative data from a repetition of this experiment.