The transient receptor potential (TRP) family is a large family of widely expressed ion channels that regulate the intracellular concentration of ions and metals and respond to various chemical and physical stimuli. TRP subfamily M member 7 (TRPM7) is unusual in that it contains both an ion channel and a kinase domain. TRPM7 is a divalent cation channel with preference for Ca²⁺ and Mg²⁺. It is required for the survival of DT40 cells, a B cell line; however, deletion of TRPM7 in T cells does not impair their development. We found that expression of TRPM7 was required for B cell development in mice. Mice that lacked TRPM7 in B cells failed to generate peripheral B cells because of a developmental block at the pro-B cell stage. The loss of TRPM7 kinase activity alone did not affect the proportion of peripheral mature B cells or the development of B cells in the bone marrow. However, supplementation with a high concentration of extracellular Mg²⁺ partially rescued the development of TRPM7-deficient B cells in vitro. Thus, our findings identify a critical role for TRPM7 ion channel activity in B cell development.

瞬时受体电位（TRP）家族是一个广泛表达的离子通道家族，可调节离子和金属的细胞内浓度并响应各种化学和物理刺激。TRP亚家族M成员7（TRPM7）不寻常，因为它同时包含离子通道和激酶结构域。TRPM7是一个二价阳离子通道，优先选择Ca ²⁺和Mg ²⁺。它是B细胞系DT40细胞存活所必需的。然而，T细胞中TRPM7的缺失不会损害它们的发育。我们发现，TRPM7的表达是小鼠B细胞发育所必需的。在B细胞中缺乏TRPM7的小鼠由于在pro B细胞阶段的发育阻滞而无法产生外周B细胞。单独的TRPM7激酶活性丧失不会影响外周成熟B细胞的比例或骨髓中B细胞的发育。但是，补充高浓度的细胞外Mg ^2+可以部分挽救TRPM7缺陷型B细胞的体外发育。因此，我们的发现确定了TRPM7离子通道活性在B细胞发育中的关键作用。