Inactivation of TRPM7 kinase activity does not impair its channel function in mice

Taku Kaitsuka, Chiaki Katagiri, Pavani Beesetty, Kenji Nakamura, Siham Hourani, Kazuhito Tomizawa, J. Ashot Kozak, Masayuki Matsushita

研究成果査読

60 被引用数 (Scopus)

抄録

Transient receptor potential (TRP) family channels are involved in sensory pathways and respond to various environmental stimuli. Among the members of this family, TRPM7 is a unique fusion of an ion channel and a C-terminus kinase domain that is highly expressed in immune cells. TRPM7 serves as a key molecule governing cellular Mg 2+ homeostasis in mammals since its channel pore is permeable to Mg 2+ ions and can act as a Mg 2+ influx pathway. However, mechanistic links between its kinase activity and channel function have remained uncertain. In this study, we generated kinase inactive knock-in mutant mice by mutagenesis of a key lysine residue involved in Mg 2+-ATP binding. These mutant mice were normal in development and general locomotor activity. In peritoneal macrophages isolated from adult animals the basal activity of TRPM7 channels prior to cytoplasmic Mg 2+ depletion was significantly potentiated, while maximal current densities measured after Mg 2+ depletion were unchanged in the absence of detectable kinase function. Serum total Ca 2+ and Mg 2+ levels were not significantly altered in kinase-inactive mutant mice. Our findings suggest that abolishing TRPM7 kinase activity does not impair its channel activity and kinase activity is not essential for regulation of mammalian Mg 2+ homeostasis.

本文言語English
論文番号5718
ジャーナルScientific reports
4
DOI
出版ステータスPublished - 7月 17 2014
外部発表はい

ASJC Scopus subject areas

  • 一般

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