Transient receptor potential channels: Emerging roles in health and disease

摘要

superfamily of related ion channel proteins that tend to exhibit relatively non-selective permeability to divalent cations (Nilius et al., 2007). The mammalian TRP superfamily consists of more than 28 TRP genes each encoding a distinct channel. The superfamily has been subdivided into six main subfamilies: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), and the TRPA (ankyrin) groups (Nilius et al., 2007). The discovery of TRP channels was related to one of the earliest described channelopathies in Drosophila melanogaster, the most commonly used genetic model. These are diseases caused by the altered function of an ion channel, its subunits or proteins that regulate it (Hoffman, 1995; Ashcroft, 2005, 2006). Channelopathies1 may be either congenital (often resulting from a mutation or mutations in the encoding genes) or acquired (often resulting from autoimmune attack on an ion channel) (Buckley and Vincent, 2005; Vincent et al., 2006). There is an ever-increasing number of clinical states that are caused by mutations in ion channels (Lehmann-Horn and Rüdel, 1996; Sanguinetti and Spector, 1997; Ptácek, 1998). The mutation that led to the discovery of TRP channels was in the trp mutant strain of Drosophila. Phototransduction in this species involves activation of membrane cation channels leading to a depolarising current. The mutant Drosophila lack a functional copy of trp gene and display a transient current in response to light, in contrast to the sustained light-induced current in wild-type flies (Cosens and Manning, 1969). This is why the mutant strain was termed trp, for transient receptor potential.