![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=1735508600&Signature=Kp8sYym~oLajfAX0~hqoQxtj9j3Bgh8KRwEu7WlJBXNAuuNHSqiWHVkvqvfmpMzFD6wV2dolioBjDtI~UnryKkpSejPx7r9ftP6gb91~zfbO9~tkqy6HqHe-xwtQeCZR2e7uPzWo~iTOWtEOFYyYvhhfOsuqMXtvrg38Zl8zjxsG8hZrP8zM~-bx-wWmTUG33O5R5NeSUX~rp9vp3pXBEkX8imP4Tzrpjg~BImwj8FaePUxvQfeNALwgP2HNrdK1S6H1ij6i19yDSPCNAm74g8FinN6Lpe0vw8cvA73d9nUXwlxtm5I95a6L4jJ8YfQMjySlOrqRU9cTlCaa2Es6QA__&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.
