Trpm6

Abstract

TRPM6 is a bifunctional protein comprising a TRP cation channel segment covalently linked to an α-type serine/threonine protein kinase. TRPM6 is expressed in the intestinal and renal epithelial cells. Loss-of-function mutations in the human TRPM6 gene give rise to hypomagnesemia with secondary hypocalcemia (HSH), suggesting that the TRPM6 channel kinase plays a central role in systemic Mg(2+) homeostasis. In contrast, Trpm6 null mice show a delay in prenatal development, neural tube defects, and prenatal death. Possible functions of TRPM6 in prenatal and adult organisms will be discussed in this chapter.

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

“…The ubiquitously-expressed TRPM6/M7 channels are fusion proteins, comprised of the traditional ion channel transmembrane domains coupled to an enzymatically active α-kinase domain (252, 430). While selective for divalent cations over monovalent cations, TRPM6/M7 have a fivefold greater selectivity for Mg 2+ over Ca 2+ and thus are key to Mg 2+ homeostasis (1633).…”

TRPM7 is a molecular substrate of ATP-evoked P2X7-like currents in tumor cells

“…TRPM6, the closest phylogenetic relative of TRPM7, is mainly expressed in the kidney, the intestine, and the testis and shares important regulatory properties with TRPM7. These include the chanzyme structure, as well as the regulation by intracellular Mg 2+ and extracellular DICs (Chubanov and Gudermann, 2014). There is ongoing debate as to whether TRPM6 can form functional channels on its own (Chubanov and Gudermann, 2014).…”

“…These include the chanzyme structure, as well as the regulation by intracellular Mg 2+ and extracellular DICs (Chubanov and Gudermann, 2014). There is ongoing debate as to whether TRPM6 can form functional channels on its own (Chubanov and Gudermann, 2014). If coexpressed with TRPM7, TRPM6 can form functional heteromeric channel complexes (Chubanov et al, 2004;Li et al, 2006).…”

Hereditary tubulopathy in the practice of adult nephrology. Case report

“…Одной из отличительных черт СГ является развитие выраженной гипокальциурии, возникающей в результате пассивной реабсорбции кальция в проксимальных канальцах вследствие усиления обратного всасывания натрия там же изза сокращения эффективного объема внеклеточной жидкости. Также для СГ характерна гипомагниемия, возникающая вследствие уменьшения активности TRPM6 (transient receptor potential cation channel subfamily M member 6), расположенного в дистальном извитом канальце, что ведет к значительным почечным потерям магния [6]. Выраженная гипомагниемия ведет к развитию хондрокальциноза, симптомами которого являются отек, покраснение и болезненность в пораженных суставах.…”