Normal activation of MAPKs and AKT by LPS, BCR, and SDF-1, and impaired activation of Pyk-2 by SDF-1 in Rap1b-deficient B cells. (A) LPS-induced activation of MAPK family members ERK, p38, and JNK and AKT in wild-type and Rap1b-deficient B cells. Sorted MZ B cells from the spleen of wild-type (+/+) and Rap1b-deficient (−/−) mice were stimulated with LPS for the indicated times. The cells were lysed, and cell lysates were subjected to direct Western blot analysis with anti–phospho-ERK, anti–phospho-p38, anti–phospho-JNK, anti–phospho-AKT, or anti-Actin antibodies. The figure shown is representative of 2 independent analyses. (B) BCR-induced activation of MAPK family members ERK, p38, and JNK and AKT in wild-type and Rap1b-deficient B cells. Sorted FO B cells from the spleen of wild-type and Rap1b-deficient mice were stimulated with anti-IgM antibody for the indicated times. The cells were lysed, and cell lysates were subjected to direct Western blot analysis with anti–phospho-ERK, anti–phospho-p38, anti–phospho-JNK, anti–phospho-AKT, or anti-Actin antibodies. The figure shown is representative of 2 independent analyses. (C) SDF-1–induced activation of ERK, AKT, and Pyk-2 in wild-type and Rap1b-deficient B cells. Purified B cells from the spleen of wild-type and Rap1b-deficient mice were stimulated with SDF-1 for the indicated times. The cells were lysed and cell lysates were subjected to direct Western blot analysis with anti–phospho-ERK, anti–phospho-AKT, anti–phospho-Pyk-2, anti–Pyk-2, or anti-Actin antibodies. The figure shown is representative of 5 independent analyses.