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  1. Article ; Online: Reply to: How Many SARS-CoV-2 "Viroporins" Are Really Ion Channels?

    Toft-Bertelsen, Trine L / Jeppesen, Mads Gravers / Landbrug, Asante / Mujezinovic, Amer / Bentzen, Bo Hjorth / Kledal, Thomas Nitschke / Rosenkilde, Mette Marie

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 860

    MeSH term(s) COVID-19 ; Humans ; Ion Channels ; SARS-CoV-2 ; Viral Proteins/metabolism ; Viroporin Proteins
    Chemical Substances Ion Channels ; Viral Proteins ; Viroporin Proteins
    Language English
    Publishing date 2022-08-25
    Publishing country England
    Document type Letter ; Comment
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-03670-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Publisher Correction: Reply to: How many SARS-CoV-2 "viroporins" are really ion channels?

    Toft-Bertelsen, Trine L / Jeppesen, Mads Gravers / Landbrug, Asante / Mujezinovic, Amer / Bentzen, Bo Hjorth / Kledal, Thomas Nitschke / Rosenkilde, Mette Marie

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 1017

    Language English
    Publishing date 2022-09-27
    Publishing country England
    Document type Published Erratum
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-03982-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Author Correction: Amantadine inhibits known and novel ion channels encoded by SARS-CoV-2 in vitro.

    Toft-Bertelsen, Trine Lisberg / Jeppesen, Mads Gravers / Tzortzini, Eva / Xue, Kai / Giller, Karin / Becker, Stefan / Mujezinovic, Amer / Bentzen, Bo Hjorth / Andreas, Loren B / Kolocouris, Antonios / Kledal, Thomas Nitschke / Rosenkilde, Mette Marie

    Communications biology

    2021  Volume 4, Issue 1, Page(s) 1402

    Language English
    Publishing date 2021-12-10
    Publishing country England
    Document type Published Erratum
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-021-02940-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Amantadine has potential for the treatment of COVID-19 because it inhibits known and novel ion channels encoded by SARS-CoV-2.

    Toft-Bertelsen, Trine Lisberg / Jeppesen, Mads Gravers / Tzortzini, Eva / Xue, Kai / Giller, Karin / Becker, Stefan / Mujezinovic, Amer / Bentzen, Bo Hjorth / B Andreas, Loren / Kolocouris, Antonios / Kledal, Thomas Nitschke / Rosenkilde, Mette Marie

    Communications biology

    2021  Volume 4, Issue 1, Page(s) 1347

    Abstract: The dire need for COVID-19 treatments has inspired strategies of repurposing approved drugs. Amantadine has been suggested as a candidate, and cellular as well as clinical studies have indicated beneficial effects of this drug. We demonstrate that ... ...

    Abstract The dire need for COVID-19 treatments has inspired strategies of repurposing approved drugs. Amantadine has been suggested as a candidate, and cellular as well as clinical studies have indicated beneficial effects of this drug. We demonstrate that amantadine and hexamethylene-amiloride (HMA), but not rimantadine, block the ion channel activity of Protein E from SARS-CoV-2, a conserved viroporin among coronaviruses. These findings agree with their binding to Protein E as evaluated by solution NMR and molecular dynamics simulations. Moreover, we identify two novel viroporins of SARS-CoV-2; ORF7b and ORF10, by showing ion channel activity in a X. laevis oocyte expression system. Notably, amantadine also blocks the ion channel activity of ORF10, thereby providing two ion channel targets in SARS-CoV-2 for amantadine treatment in COVID-19 patients. A screen of known viroporin inhibitors on Protein E, ORF7b, ORF10 and Protein 3a from SARS-CoV-2 revealed inhibition of Protein E and ORF7b by emodin and xanthene, the latter also blocking Protein 3a. This illustrates a general potential of well-known ion channel blockers against SARS-CoV-2 and specifically a dual molecular basis for the promising effects of amantadine in COVID-19 treatment. We therefore propose amantadine as a novel, cheap, readily available and effective way to treat COVID-19.
    MeSH term(s) Amantadine/pharmacology ; Amiloride/analogs & derivatives ; Amiloride/pharmacology ; Antiviral Agents/pharmacology ; Ion Channels/physiology ; Rimantadine/pharmacology ; SARS-CoV-2/drug effects ; Viral Proteins/physiology
    Chemical Substances Antiviral Agents ; Ion Channels ; Viral Proteins ; Rimantadine (0T2EF4JQTU) ; 5-(N,N-hexamethylene)amiloride (1428-95-1) ; Amiloride (7DZO8EB0Z3) ; Amantadine (BF4C9Z1J53)
    Language English
    Publishing date 2021-12-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-021-02866-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: High incidence of functional ion-channel abnormalities in a consecutive Long QT cohort with novel missense genetic variants of unknown significance.

    Steffensen, Annette Buur / Refaat, Marwan M / David, Jens-Peter / Mujezinovic, Amer / Calloe, Kirstine / Wojciak, Julianne / Nussbaum, Robert L / Scheinman, Melvin M / Schmitt, Nicole

    Scientific reports

    2015  Volume 5, Page(s) 10009

    Abstract: The Long QT syndrome (LQTS) is a disorder characterized by a prolongation of the QT interval and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death. Our objective was to (1) determine the incidence of ...

    Abstract The Long QT syndrome (LQTS) is a disorder characterized by a prolongation of the QT interval and a propensity to ventricular tachyarrhythmias, which may lead to syncope, cardiac arrest, or sudden death. Our objective was to (1) determine the incidence of variants with unknown significance (VUS) in a cohort of consecutive LQTS patients and (2) to determine the percentage of those with novel missense VUS that have demonstrable functional channel abnormalities from a single referral center. We performed genetic screening of candidate genes in 39 probands with a diagnosis of LQTS to identify mutations and variants. Seven variants of unknown significance were identified, six were missense variants and one was a splice site variant. We investigated the six novel missense VUS in five patients; three missense variants in KCNQ1 (L236R, W379R, Y522S) and three missense variants in KCNH2 (R35W, S620G, V491I). We employed two-electrode voltage-clamp experiments in Xenopus laevis oocytes and confocal imaging to characterize the novel missense mutations functionally. We revealed electrophysiological and trafficking loss-of-function phenotypes. This report emphasizes the frequency of adverse channel function in patients with LQTS and the importance of heterologous studies to define channel function.
    MeSH term(s) Amino Acid Substitution ; Animals ; Cohort Studies ; ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels/genetics ; Female ; Humans ; KCNQ1 Potassium Channel/genetics ; Long QT Syndrome/genetics ; Male ; Mutation, Missense ; Xenopus laevis
    Chemical Substances ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels ; KCNH2 protein, human ; KCNQ1 Potassium Channel ; KCNQ1 protein, human
    Language English
    Publishing date 2015-06-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep10009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: IKs Gain- and Loss-of-Function in Early-Onset Lone Atrial Fibrillation.

    Steffensen, Annette Buur / Refsgaard, Lena / Andersen, Martin Nybo / Vallet, Cecilia / Mujezinovic, Amer / Haunsø, Stig / Svendsen, Jesper Hastrup / Olesen, Søren-Peter / Olesen, Morten Salling / Schmitt, Nicole

    Journal of cardiovascular electrophysiology

    2015  Volume 26, Issue 7, Page(s) 715–723

    Abstract: Introduction: Atrial fibrillation (AF) is the most frequent cardiac arrhythmia. The potassium current IKs is essential for cardiac repolarization. Gain-of-function mutation in KCNQ1, the gene encoding the pore-forming α-subunit of the IKs channel (KV 7 ... ...

    Abstract Introduction: Atrial fibrillation (AF) is the most frequent cardiac arrhythmia. The potassium current IKs is essential for cardiac repolarization. Gain-of-function mutation in KCNQ1, the gene encoding the pore-forming α-subunit of the IKs channel (KV 7.1), was the first ion channel dysfunction to be associated with familial AF. We hypothesized that early-onset lone AF is associated with a high prevalence of mutations in KCNQ1.
    Methods and results: We bidirectionally sequenced the entire coding sequence of KCNQ1 in 209 unrelated patients with early-onset lone AF (<40 years) and investigated the identified mutations functionally in a heterologous expression system. We found 4 nonsynonymous KCNQ1 mutations (A46T, R195W, A302V, and R670K) in 4 unrelated patients (38, 31, 39, and 36 years, respectively). None of the mutations were present in the control group (n = 416 alleles). No other mutations were found in genes previously associated with AF. The mutations A46T, R195W, and A302V have previously been associated with long-QT syndrome. In line with previous reports, we found A302V to display a pronounced loss-of-function of the IKs current, while the other mutants exhibited a gain-of-function phenotype.
    Conclusions: Mutations in the IKs channel leading to gain-of-function have previously been described in familial AF, yet this is the first time a loss-of-function mutation in KCNQ1 is associated with early-onset lone AF. These findings suggest that both gain-of-function and loss-of-function of cardiac potassium currents enhance the susceptibility to AF.
    MeSH term(s) Action Potentials ; Adolescent ; Adult ; Atrial Fibrillation/diagnosis ; Atrial Fibrillation/genetics ; Atrial Fibrillation/metabolism ; Atrial Fibrillation/physiopathology ; Atrial Fibrillation/therapy ; Case-Control Studies ; Cell Line ; DNA Mutational Analysis ; Denmark ; Electrocardiography ; Female ; Genetic Predisposition to Disease ; Heart Rate ; Humans ; KCNQ1 Potassium Channel/genetics ; KCNQ1 Potassium Channel/metabolism ; Male ; Mutation ; Myocytes, Cardiac/metabolism ; Phenotype ; Potassium/metabolism ; Transfection ; Young Adult
    Chemical Substances KCNQ1 Potassium Channel ; KCNQ1 protein, human ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2015-07
    Publishing country United States
    Document type Case Reports ; Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025989-2
    ISSN 1540-8167 ; 1045-3873
    ISSN (online) 1540-8167
    ISSN 1045-3873
    DOI 10.1111/jce.12666
    Database MEDical Literature Analysis and Retrieval System OnLINE

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