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  1. Article: The proteostasis interactomes of trafficking-deficient K

    Egly, Christian L / Barny, Lea / Do, Tri / McDonald, Eli F / Plate, Lars / Knollmann, Bjorn C

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Introduction: The voltage gated potassium ion channel K : Methods: We used affinity-purification coupled with tandem mass tag-based quantitative mass spectrometry to assess protein interaction changes in human embryonic kidney (HEK293) cells ... ...

    Abstract Introduction: The voltage gated potassium ion channel K
    Methods: We used affinity-purification coupled with tandem mass tag-based quantitative mass spectrometry to assess protein interaction changes in human embryonic kidney (HEK293) cells expressing wild-type (WT) K
    Resultsa: We identified 573 core K
    Conclusion: Our report characterizes the proteostasis network of K
    Language English
    Publishing date 2024-01-31
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.31.574410
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A High-Throughput Screening Assay to Identify Drugs that Can Treat Long QT Syndrome Caused by Trafficking-Deficient K

    Egly, Christian L / Blackwell, Daniel J / Schmeckpeper, Jeffrey / Delisle, Brian P / Weaver, C David / Knollmann, Björn C

    Molecular pharmacology

    2022  Volume 101, Issue 4, Page(s) 236–245

    Abstract: Loss-of-function (LOF) variants in the ... ...

    Abstract Loss-of-function (LOF) variants in the K
    MeSH term(s) ERG1 Potassium Channel/genetics ; ERG1 Potassium Channel/metabolism ; Ether-A-Go-Go Potassium Channels/metabolism ; HEK293 Cells ; High-Throughput Screening Assays ; Humans ; Long QT Syndrome/drug therapy ; Long QT Syndrome/genetics ; Thallium/metabolism
    Chemical Substances ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels ; Thallium (AD84R52XLF)
    Language English
    Publishing date 2022-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 124034-1
    ISSN 1521-0111 ; 0026-895X
    ISSN (online) 1521-0111
    ISSN 0026-895X
    DOI 10.1124/molpharm.121.000421
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: RYR2 Channel Inhibition Is the Principal Mechanism of Flecainide Action in CPVT.

    Kryshtal, Dmytro O / Blackwell, Daniel J / Egly, Christian L / Smith, Abigail N / Batiste, Suzanne M / Johnston, Jeffrey N / Laver, Derek R / Knollmann, Bjorn C

    Circulation research

    2020  Volume 128, Issue 3, Page(s) 321–331

    Abstract: Rationale: The class Ic antiarrhythmic drug flecainide prevents ventricular tachyarrhythmia in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), a disease caused by hyperactive RyR2 (cardiac ryanodine receptor) mediated calcium ...

    Abstract Rationale: The class Ic antiarrhythmic drug flecainide prevents ventricular tachyarrhythmia in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT), a disease caused by hyperactive RyR2 (cardiac ryanodine receptor) mediated calcium (Ca) release. Although flecainide inhibits single RyR2 channels in vitro, reports have claimed that RyR2 inhibition by flecainide is not relevant for its mechanism of antiarrhythmic action and concluded that sodium channel block alone is responsible for flecainide's efficacy in CPVT.
    Objective: To determine whether RyR2 block independently contributes to flecainide's efficacy for suppressing spontaneous sarcoplasmic reticulum Ca release and for preventing ventricular tachycardia in vivo.
    Methods and results: We synthesized N-methylated flecainide analogues (QX-flecainide and
    Conclusions: Flecainide remains an effective inhibitor of RyR2-mediated arrhythmogenic Ca release even when cardiac sodium channels are blocked. In mice with CPVT, sodium channel block alone did not prevent ventricular tachycardia. Hence, RyR2 channel inhibition likely constitutes the principal mechanism of antiarrhythmic action of flecainide in CPVT.
    MeSH term(s) Action Potentials ; Animals ; Anti-Arrhythmia Agents/pharmacology ; Calcium Channel Blockers/pharmacology ; Calcium Signaling ; Calsequestrin/genetics ; Calsequestrin/metabolism ; Disease Models, Animal ; Female ; Flecainide/pharmacology ; HEK293 Cells ; Heart Rate/drug effects ; Humans ; Male ; Mice, Knockout ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Phosphorylation ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism ; Sheep, Domestic ; Tachycardia, Ventricular/genetics ; Tachycardia, Ventricular/metabolism ; Tachycardia, Ventricular/physiopathology ; Tachycardia, Ventricular/prevention & control ; Voltage-Gated Sodium Channel Blockers/pharmacology ; Mice
    Chemical Substances Anti-Arrhythmia Agents ; Calcium Channel Blockers ; Calsequestrin ; Ryanodine Receptor Calcium Release Channel ; Voltage-Gated Sodium Channel Blockers ; casq2 protein, mouse ; ryanodine receptor 2. mouse ; Flecainide (K94FTS1806)
    Language English
    Publishing date 2020-12-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.120.316819
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.70: Show issues Location:
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  4. Article ; Online: Eicosanoid-Regulated Myeloid ENaC and Isolevuglandin Formation in Human Salt-Sensitive Hypertension.

    Ertuglu, Lale A / Pitzer Mutchler, Ashley / Jamison, Sydney / Laffer, Cheryl L / Elijovich, Fernando / Saleem, Mohammad / Blackwell, Daniel J / Kryshtal, Dmytro O / Egly, Christian L / Sahinoz, Melis / Sheng, Quanhu / Wanjalla, Celestine N / Pakala, Suman / Yu, Justin / Gutierrez, Orlando M / Kleyman, Thomas R / Knollmann, Björn C / Ikizler, T Alp / Kirabo, Annet

    Hypertension (Dallas, Tex. : 1979)

    2023  Volume 81, Issue 3, Page(s) 516–529

    Abstract: Background: The mechanisms by which salt increases blood pressure in people with salt sensitivity remain unclear. Our previous studies found that high sodium enters antigen-presenting cells (APCs) via the epithelial sodium channel and leads to the ... ...

    Abstract Background: The mechanisms by which salt increases blood pressure in people with salt sensitivity remain unclear. Our previous studies found that high sodium enters antigen-presenting cells (APCs) via the epithelial sodium channel and leads to the production of isolevuglandins and hypertension. In the current mechanistic clinical study, we hypothesized that epithelial sodium channel-dependent isolevuglandin-adduct formation in APCs is regulated by epoxyeicosatrienoic acids (EETs) and leads to salt-sensitive hypertension in humans.
    Methods: Salt sensitivity was assessed in 19 hypertensive subjects using an inpatient salt loading and depletion protocol. Isolevuglandin-adduct accumulation in APCs was analyzed using flow cytometry. Gene expression in APCs was analyzed using cellular indexing of transcriptomes and epitopes by sequencing analysis of blood mononuclear cells. Plasma and urine EETs were measured using liquid chromatography-mass spectrometry.
    Results: Baseline isolevuglandin
    Conclusions: Isolevuglandin formation in APCs responds to acute changes in salt intake in salt-sensitive but not salt-resistant people with hypertension, and this may be regulated by renal 14,15 EET. Baseline levels of isolevuglandin
    MeSH term(s) Humans ; Sodium Chloride, Dietary/metabolism ; Epithelial Sodium Channels/metabolism ; Hypertension ; Sodium Chloride/metabolism ; Eicosanoids ; Blood Pressure/physiology ; Lipids
    Chemical Substances Sodium Chloride, Dietary ; isolevuglandin ; Epithelial Sodium Channels ; Sodium Chloride (451W47IQ8X) ; Eicosanoids ; Lipids
    Language English
    Publishing date 2023-09-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.123.21285
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1488: Show issues Location:
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  5. Article ; Online: High-throughput discovery of trafficking-deficient variants in the cardiac potassium channel K

    Kozek, Krystian A / Glazer, Andrew M / Ng, Chai-Ann / Blackwell, Daniel / Egly, Christian L / Vanags, Loren R / Blair, Marcia / Mitchell, Devyn / Matreyek, Kenneth A / Fowler, Douglas M / Knollmann, Bjorn C / Vandenberg, Jamie I / Roden, Dan M / Kroncke, Brett M

    Heart rhythm

    2020  Volume 17, Issue 12, Page(s) 2180–2189

    Abstract: Background: KCHN2 encodes the K: Objective: The purpose of this study was to report a high-throughput, multiplexed screening method for KCNH2 genetic variants capable of measuring the cell surface abundance of hundreds of missense variants in the ... ...

    Abstract Background: KCHN2 encodes the K
    Objective: The purpose of this study was to report a high-throughput, multiplexed screening method for KCNH2 genetic variants capable of measuring the cell surface abundance of hundreds of missense variants in the resulting K
    Methods: We developed a method to quantitate K
    Results: We generated trafficking scores for 220 of 231 missense variants in the pilot region. For 5 of 5 variants, high-throughput trafficking scores validated when tested in single variant flow cytometry and confocal microscopy experiments. We further explored these results with planar patch electrophysiology and found that loss-of-trafficking variants do not produce I
    Conclusion: We describe a new method for detecting K
    MeSH term(s) Cell Line ; DNA/genetics ; DNA Mutational Analysis ; ERG1 Potassium Channel/genetics ; ERG1 Potassium Channel/metabolism ; Humans ; Long QT Syndrome/genetics ; Long QT Syndrome/metabolism ; Long QT Syndrome/physiopathology ; Mutation ; Myocardium/metabolism ; Myocardium/pathology ; Patch-Clamp Techniques
    Chemical Substances ERG1 Potassium Channel ; KCNH2 protein, human ; DNA (9007-49-2)
    Language English
    Publishing date 2020-06-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2229357-7
    ISSN 1556-3871 ; 1547-5271
    ISSN (online) 1556-3871
    ISSN 1547-5271
    DOI 10.1016/j.hrthm.2020.05.041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6278: Show issues Location:
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