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. 2013 Nov 15;27(22):2439–2444. doi: 10.1101/gad.227165.113

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© 2013 Kumar et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.

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Figure 2. — V(D)J joining can follow CSR in early B-cell lines. Cells were untreated (U) or activated with LPS+CD40L (LC) or LPS+CD40L+IL4 (LCI). Results are representative of three to nine samples from three independent experiments. (A) DC-PCR analysis of CSR in R2K2 and in clones A2 and B5. (B) STI571 treatment induces Rag1, Igκ GLT, and Irf4 expression as assessed by quantitative RT–PCR in B5 and A2 clones. (C) D_DFL16 → J_H1 CJs assessed in A2 and B5 clones transfected with empty (E) or Rag2 (R) expression constructs and the Mb1 loading control. (D, top) Treatment timeline in PA112.2 cells. (Bottom) Quantitative RT–PCR for AID and Rag2 expression. (E) Semiquantitative RT–PCR for PST γ2b and ɛ or Hprt. (F) V_κ6–23 → J_κ1 CJs and Mb1 assessed by semiquantitative PCR.