WorldCat Identities

Choveau, Frank (1980-)

Overview
Works: 2 works in 2 publications in 1 language and 2 library holdings
Roles: Author
Publication Timeline
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Most widely held works by Frank Choveau
Couplages moléculaires à l'origine de la dépendance au potentiel des canaux KCNQ1 et hERG by Frank Choveau( Book )

1 edition published in 2009 in French and held by 1 WorldCat member library worldwide

The long QT syndrome is a cardiac abnormality of cardiac leading to altered ventricular repolarization that can lead to arrhythmias, and sudden death. This syndrome exists in 2 forms: congenital and acquired. The congenital form is mostly due to a dysfunction of the six-transmembrane-domain voltage-gated potassium channel: KCNQ1. Currently, the molecular mechanisms controlling the voltage-dependency of KCNQ1 are not clearly identified. We show that the S4-S5 linker acts as a ligand binding to the S6 and stabilizing the channel closed state: peptides mimicking the S4-S5 linker inhibit KCNQ1 whereas those mimicking the S6 domain increase upregulate KCNQ1 activity. This increase in KCNQ1 activity by S6 peptides could compensate for the channel dysfunction observed in the long QT syndrome and thus represent a new therapytherapeutic approach. Off target inhibition of hERG potassium channel by many drugs can induce the acquired form of the long QT syndrome. This inhibition may be favored by the trapping of these molecules in the channel pore of the channel following the closure of the gate activation. To check this hypothesis, we blocked this gate in the open state. Moreover, if the activation and inactivation are coupled, a reduced inhibition of hERG may be due to inactivation rather than activation. We show that (i) activation and inactivation are not coupled, and that (ii) stabilizing of the activation gate is responsible for this inhibition
Couplages moléculaires à l'origine de la dépendance au potentiel des canaux KCNQ1 et hERG by Frank Choveau( )

1 edition published in 2009 in French and held by 1 WorldCat member library worldwide

The long QT syndrome is a cardiac abnormality of cardiac leading to altered ventricular repolarization that can lead to arrhythmias, and sudden death. This syndrome exists in 2 forms: congenital and acquired. The congenital form is mostly due to a dysfunction of the six-transmembrane-domain voltage-gated potassium channel: KCNQ1. Currently, the molecular mechanisms controlling the voltage-dependency of KCNQ1 are not clearly identified. We show that the S4-S5 linker acts as a ligand binding to the S6 and stabilizing the channel closed state: peptides mimicking the S4-S5 linker inhibit KCNQ1 whereas those mimicking the S6 domain increase upregulate KCNQ1 activity. This increase in KCNQ1 activity by S6 peptides could compensate for the channel dysfunction observed in the long QT syndrome and thus represent a new therapytherapeutic approach. Off target inhibition of hERG potassium channel by many drugs can induce the acquired form of the long QT syndrome. This inhibition may be favored by the trapping of these molecules in the channel pore of the channel following the closure of the gate activation. To check this hypothesis, we blocked this gate in the open state. Moreover, if the activation and inactivation are coupled, a reduced inhibition of hERG may be due to inactivation rather than activation. We show that (i) activation and inactivation are not coupled, and that (ii) stabilizing of the activation gate is responsible for this inhibition
 
Audience Level
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Audience Level
1
  General Special  
Audience level: 0.94 (from 0.94 for Couplages ... to 0.94 for Couplages ...)

Languages
French (2)