ASK1 promotes apoptosis of normal and malignant plasma cells

摘要: Although the overproduction of immunoglobulins by short-lived plasma cells accompanying an immune response links with their apoptosis, how long-lived adapt to ensure longevity in this context is obscure. Here, we show that apoptosis signal–regulating kinase 1 (ASK1) contributes because ASK1 activity was induced during differentiation cells, and, when produced ASK1-deficient mice, these survived better than those control mice. Moreover, antigen-specific generated immunization accumulated suggesting also plays a negative role survival cells. In malignant transcription directly suppressed B lymphocyte–induced maturation protein-1 (Blimp-1). The expression and Blimp-1 showed inverse correlation between normal human mature bone marrow from patients multiple myeloma (MM). Suppression crucial for cell its enforced MM caused vitro lowered load xenograft animal model; furthermore, alteration affected survival. Our findings indicate novel mechanism underlying regulation ASK1.