![Figure 3. Reduced proliferation and survival of TAK1-deficient B cells. (A) Impaired thymidine incorporation of TAK1-deficient B cells in response to anti-IgM or LPS. Splenic immature (AA4.1+) and mature (AA4.1−) B cells were purified from CD19CreTak1+/+ and CD19CreTak1fl/fl mice and then stimulated with anti-IgM, anti-IgM + IL-4, or LPS. Proliferative responses were determined by [3H]thymidine incorporation. (B) Cell-cycle profile of TAK1-deficient immature B cells in response to anti-IgM or LPS. After stimulation, AA4.1+ B cells were collected, stained with PI, and analyzed for cell-cycle profile by FACS. The percentages of subG0 populations in total cells and percentages of G0/G1 and S + G2/M population in live cells are indicated. (C) Cell-cycle profile of TAK1-deficient mature B cells in response to anti-IgM or LPS. After stimulation, AA4.1− B cells were collected, stained with PI, and analyzed for cell-cycle profile by FACS. The percentages of subG0 populations in total cells and percentages of G0/G1, and S + G2/M population in live cells are indicated. (D) Reduced survival of TAK1-deficient B cells in response to anti-IgM or LPS. AA4.1+ and AA4.1− B cells from CD19CreTak1+/+ and CD19CreTak1fl/fl mice were stimulated with anti-IgM + IL-4 or LPS. At the indicated time points, cell survival rates were determined by PI staining. Data are representative of 5 (A) or 3 (B-D) independent experiments.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/113/19/10.1182_blood-2008-08-176057/7/zh80170934270003.jpeg?Expires=1722715293&Signature=Pwc28~-nawOosHvHhxW1nLC6UOaHEiZ6zeoeyTPb8YGqJ9hg77nkjNDns1rZNe2HUmireRcQPw9Dym4d25pO985anHNwwqTaaJt~wlS7DUzFriFCpNR79ZGxnV4NkV7gyDqpIG9kjrnovXx3t2pz8OhlH8Iz17aXjQn6U89zzRUEZ-f1hQ604uBnj1hwWSs6PsBiUS2hr1ml9dr7rREc1xGuF9CClbETrvjRrFoMTj43cRhYja4WP6EuejWLK9YJsengJd2xPbD5c0US6Q2S6emq-j423lI1W~IYwapqNqNwE8y9nHrTTW0WqQZU6H~FsZvlostsAiL4ypDfXfq46g__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Reduced proliferation and survival of TAK1-deficient B cells. (A) Impaired thymidine incorporation of TAK1-deficient B cells in response to anti-IgM or LPS. Splenic immature (AA4.1+) and mature (AA4.1−) B cells were purified from CD19CreTak1+/+ and CD19CreTak1fl/fl mice and then stimulated with anti-IgM, anti-IgM + IL-4, or LPS. Proliferative responses were determined by [3H]thymidine incorporation. (B) Cell-cycle profile of TAK1-deficient immature B cells in response to anti-IgM or LPS. After stimulation, AA4.1+ B cells were collected, stained with PI, and analyzed for cell-cycle profile by FACS. The percentages of subG0 populations in total cells and percentages of G0/G1 and S + G2/M population in live cells are indicated. (C) Cell-cycle profile of TAK1-deficient mature B cells in response to anti-IgM or LPS. After stimulation, AA4.1− B cells were collected, stained with PI, and analyzed for cell-cycle profile by FACS. The percentages of subG0 populations in total cells and percentages of G0/G1, and S + G2/M population in live cells are indicated. (D) Reduced survival of TAK1-deficient B cells in response to anti-IgM or LPS. AA4.1+ and AA4.1− B cells from CD19CreTak1+/+ and CD19CreTak1fl/fl mice were stimulated with anti-IgM + IL-4 or LPS. At the indicated time points, cell survival rates were determined by PI staining. Data are representative of 5 (A) or 3 (B-D) independent experiments.
