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- W1599519762 abstract "Voltage-gated ion channels make up a superfamily ofmembrane proteins involved in selectively or non-selectivelyconducting charged ions, which can carry current in and out ofcells, in response to changes in membrane voltage. Currents carriedby ion channels influence the voltage across the cell membrane,which can trigger changes in the conductance of neighboringvoltage-gated channels. In this way, signals, measured as transientchanges in voltage called action potentials, can be sent throughand between cells in order to transmit information quickly andefficiently throughout excitable systems. My thesis work focuses onelucidating the mechanisms underlying the voltage-dependent gatingof a member of the voltage gated potassium (Kv) channel family,KCNQ1 (Kv7.1). Like other members of the voltage gated potassiumfamily, the KCNQ1 channel is made up of four subunits, eachcontaining a voltage sensing domain and a pore-forming domain.Tetrameric channels form with a single central pore domain, andfour structurally independent voltage sensing domains. KCNQ1 playsroles both in maintenance of the membrane potential (it forms aleak current in epithelial cells throughout the body) as well as avery important role in resting membrane potential reestablishment(it forms a slowly activating current important in action potentialrepolarization in cardiac cells). In order to serve these variedfunctions, KCNQ1 displays uniquely flexible gating properties amongKv channels. Evidence of this flexibility is found in theobservation that the presence or absence of various beta subunitscan cause the channel to be non-conducting, slowly activating witha large conductance, quickly activating with a small conductance,or constitutively active. My thesis project has been to unravel themechanisms underlying these very different phenotypes, focusing onthe role of the voltage sensor and its coupling to the channelgate. Most of this work focuses on the role of KCNQ1 in the heart,where it comprises the alpha subunit of the slowly activatingdelayed rectifier current, IKs. This current plays a major role inrepolarization of the cardiac action potential, evidenced in partby its major role in shortening the action potential in the facesympathetic stimulation, which leads to phosphorylation-inducedincrease in IKs current. Further evidence for the importance of IKsto proper cardiac function is found through the identification ofmany mutations to IKs that result in cardiac arrhythmia, mostnotably Long QT syndrome, which results from loss of IKs currentand an associated prolongation of the cardiac action potential. Inaddition, gain-of-function IKs mutations have been implicated inShort QT Syndrome and an inherited form of atrial fibrillation. Inorder to understand mechanisms underlying the physiological andpathophysiological functions of IKs, a more complete picture of itsstructure and function are needed. One major goal in the pursuit ofa more complete characterization of IKs is to understand theinteraction between the…" @default.
- W1599519762 created "2016-06-24" @default.
- W1599519762 creator A5043817110 @default.
- W1599519762 date "2012-01-01" @default.
- W1599519762 modified "2023-09-23" @default.
- W1599519762 title "Characterization of cardiac IKs channel gating using voltage clamp fluorometry" @default.
- W1599519762 doi "https://doi.org/10.7916/d82b950k" @default.
- W1599519762 hasPublicationYear "2012" @default.
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