Deletion of Trpm7 disrupts embryonic development and thymopoiesis without altering Mg2+ homeostasis.
Deletion of Trpm7 disrupts embryonic development and thymopoiesis without altering Mg2+ homeostasis.
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DOI：
10.1126/science.1163493
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发表时间：
2008-10-31
期刊：
影响因子：
--
通讯作者：
Clapham DE
中科院分区：
文献类型：
--
作者：
Jin J;Desai BN;Navarro B;Donovan A;Andrews NC;Clapham DE
瞬时受体电位-褪黑抑素样7 （Trpm7）基因编码一种具有离子通道和激酶功能的蛋白质。TRPM7被认为是脊椎动物细胞Mg2+稳态所必需的。小鼠Trpm7的缺失揭示了它对胚胎发育至关重要。在T细胞谱系中，Trpm7的组织特异性缺失破坏了胸腺生成，导致胸腺细胞在双阴性阶段发育阻滞和胸腺髓细胞的逐渐耗尽。然而，T细胞中Trpm7的缺失并不影响Mg2+的急性摄取或细胞总Mg2+的维持。trpm7缺陷胸腺细胞表现出许多胸腺上皮细胞分化和维持所必需的生长因子合成失调。当Trpm7在胸腺细胞中被破坏时，胸腺髓细胞失去了信号换能器和转录激活因子3活性，这就是它们的损耗。
The gene transient receptor potential-melastatin-like 7 (Trpm7) encodes a protein that functions as an ion channel and a kinase. TRPM7 has been proposed to be required for cellular Mg2+ homeostasis in vertebrates. Deletion of mouse Trpm7 revealed that it is essential for embryonic development. Tissue-specific deletion of Trpm7 in the T cell lineage disrupted thymopoiesis, which led to a developmental block of thymocytes at the double-negative stage and a progressive depletion of thymic medullary cells. However, deletion of Trpm7 in T cells did not affect acute uptake of Mg2+ or the maintenance of total cellular Mg2+. Trpm7-deficient thymocytes exhibited dysregulated synthesis of many growth factors that are necessary for the differentiation and maintenance of thymic epithelial cells. The thymic medullary cells lost signal transducer and activator of transcription 3 activity, which accounts for their depletion when Trpm7 is disrupted in thymocytes.
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影响因子：
3.8
作者：
Li, Mingjiang;Jiang, Jianmin;Yue, Lixia
通讯作者：
Yue, Lixia
DOI：
10.1085/jgp.20028551
发表时间：
2002-05
期刊：
The Journal of general physiology
影响因子：
--
作者：
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通讯作者：
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影响因子：
29
作者：
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通讯作者：
Andrews, NC
影响因子：
20.3
作者：
Erickson, M;Morkowski, S;Farr, AG
通讯作者：
Farr, AG
影响因子：
4.8
作者：
Cernkovich, Erin R.;Deng, Jianbei;Harp, Joyce B.
通讯作者：
Harp, Joyce B.