title: TRPC channels: interacting proteins.
abstract: TRP channels, in particular the TRPC and TRPV subfamilies, have emerged as important constituents of the receptor-activated Ca2+ influx mechanism triggered by hormones, growth factors, and neurotransmitters through activation ofphospholipase C (PLC). Several TRPC channels are also activated by passive depletion of endoplasmic reticulum (ER) Ca2+. Although in several studies the native TRP channels faithfully reproduce the respective recombinant channels, more often the properties of Ca2+ entry and/or the store-operated current are strikingly different from that of the TRP channels expressed in the same cells. The present review aims to discuss this disparity in the context of interaction of TRPC channels with auxiliary proteins that may alter the permeation and regulation of TRPC channels.
authors.affiliation: Department of Biological Sciences University of Pittsburgh, Pittsburgh, PA 15260, USA.
authors.forename: K
authors.initials: K
authors.lastname: Kiselyov
authors.forename: D M
authors.initials: DM
authors.lastname: Shin
authors.forename: J Y
authors.initials: JY
authors.lastname: Kim
authors.forename: J P
authors.initials: JP
authors.lastname: Yuan
authors.forename: S
authors.initials: S
authors.lastname: Muallem
mesh_terms: D000818:Animals; D001711:Biotransformation / Q000187:drug effects / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D011506:Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology*; D011994:Recombinant Proteins / Q000378:metabolism; D050052:TRPC Cation Channels / Q000378:metabolism / Q000502:physiology*
chemical_list: D011506:Proteins; D011994:Recombinant Proteins; D050052:TRPC Cation Channels