While many potential mechanotransduction channels have been disregarded outright, a few have proved promising and others still remain a possibility. here are a few of the likeliest candidates, past and present. Those that remain a possibility are marked with an asterisk (*).
|CHANNEL||EVIDENCE FOR||EVIDENCE AGAINST||REFERENCES|
|Nompc, transient receptor potential (TRP) channel in Drosophila||Mutants have vestibular defects and altered transduction current||NompC gene is not present in mammals||Science, 287:2229-34, 2000|
|TRPA1, mammalian TRP channel||Antibody to channel localizes to stereocilia tips, and inhibition of the channel alters transduction current||Knockout mice have no hearing disabilities||Nature, 432:723-30, 2004|
|ENaC, family of amiloridesensitive epithelial sodium channels||C. elegans mutants are defective for mechanosensation; protein localized to hair cell stereocilia; also present in sensory endings in skin||Conductance too low; knockout mice have normal hearing||J Physiol-London, 558:659-69, 2004|
|TRPML3*, mammalian TRP channel||Mutant mice are born deaf; gene expressed in hair cells||No physiologic evidence to support channel's role in transduction||PNAS, 99:14994-9, 2002|
|TRPP*, mammalian channel; responsible for polycystic kidney disease||Involved in mechanosensation in kidney epithelial cells; conductance comparable to mechanotransduction channel||Unknown whether hair cells express channel||J Neurosci, 26:10992-1000, 2006|