TRPs, mammalian homologs of the Drosophilatransient receptor potential (trp) protein, are ion channels that are thought to mediate capacitative calcium entry into the cell. TRP-PLIK is a protein that is both an ion channel and a kinase. As a channel, it conducts calcium and monovalent cations to depolarize cells and increase intracellular calcium. As a kinase, it is capable of phosphorylating itself and other substrates. The kinase activity is necessary for channel function, as shown by its dependence on intracellular ATP and by the kinase mutants.[supplied by OMIM]
^Baldoli, Erika; Maier, Jeanette A. M. (20 December 2011). "Silencing TRPM7 mimics the effects of magnesium deficiency in human microvascular endothelial cells". Angiogenesis15 (1): 47–57. doi:10.1007/s10456-011-9242-0.
Chubanov V, Gudermann T, Schlingmann KP (2006). "Essential role for TRPM6 in epithelial magnesium transport and body magnesium homeostasis.". Pflugers Arch.451 (1): 228–34. doi:10.1007/s00424-005-1470-y. PMID16075242.
Clapham DE, Julius D, Montell C, Schultz G (2006). "International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels.". Pharmacol. Rev.57 (4): 427–50. doi:10.1124/pr.57.4.6. PMID16382100.