B cell development demands ion flux
In various immune cell types, the divalent cation channel-kinase TRPM7 regulates cell survival, migration, and effector functions. Krishnamoorthy et al. found that B cell–specific deletion of TRPM7 blocked the development of mature peripheral B cells in mice. Loss of TRPM7, but not its kinase activity, increased the apoptosis of B cell precursors in the bone marrow. Supplementation with extracellular magnesium rescued the development of TRPM7-deficient B cells in vitro. These data suggest that the ion channel activity of TRPM7 is required for B cell development.
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