Results 81 to 90 of about 17,722 (214)
Mechanisms of hERG Potassium Channel Enhancers [PDF]
Mutations in the human Ether-a-go-go related gene (hERG) potassium channel and hERG channel blockers offer tools for studying structural, biophysical and functional properties of the channel. However, the current understanding of how the hERG channel opens and closes is still incomplete. Here, we used alternative chemical tools, hERG channel enhancers,
Lin, Chia-Wei +4 more
openaire +1 more source
14‐3‐3 proteins: Regulators of cardiac excitation–contraction coupling and stress responses
Abstract figure legend 14‐3‐3 protein interactions in cardiac regulation. Schematic representation of 14‐3‐3 binding partners in excitation–contraction coupling, transcriptional regulation/development and stress response pathways. Asterisks indicate targets where the exact 14‐3‐3 binding site is unknown.
Heather C. Spooner, Rose E. Dixon
wiley +1 more source
Ion channels: structural basis for function and disease. [PDF]
Ion channels are ubiquitous proteins that mediate nervous and muscular function, rapid transmembrane signaling events, and ionic and fluid balance. The cloning of genes encoding ion channels has led to major strides in understanding the mechanistic basis
Goldstein, SA
core +1 more source
Caenorhabditis elegans as an in vivo model system for human inherited primary arrhythmia syndromes
Abstract figure legend Most genes involved in inherited primary arrhythmia syndromes (IPAS) are conserved in Caenorhabditis elegans, where genetic manipulation enables functional characterization of variants, identification of regulatory proteins, and in vivo drug testing.
Antoine Delinière +6 more
wiley +1 more source
Long-Chain Acylcarnitines Regulate the hERG Channel
In some pathological conditions carnitine concentration is high while in others it is low. In both cases,cardiac arrhythmias can occur and lead to sudden cardiac death. It has been proposed that in ischaemia, acylcarnitine (acyl-CAR), but not carnitine, is involved in arrhythmias through modulation of ionic currents. We studied the effects of acyl-CARs
Ferro, Fabio +7 more
openaire +5 more sources
Abstract Aims Paroxetine is a selective serotonin reuptake inhibitor (SSRI), approved for treatment of major depressive disorder and anxiety disorders. Some SSRIs are known to prolong the QT interval; however, clinical evidence to establish a lack of association between paroxetine and corrected QT interval (QTc) prolongation is limited. Therefore, this
Sven C. van Dijkman +6 more
wiley +1 more source
Ion Conduction through the hERG Potassium Channel
The inward rectifier voltage-gated potassium channel hERG is of primary importance for the regulation of the membrane potential of cardiomyocytes. Unlike most voltage-gated K(+)-channels, hERG shows a low elementary conductance at physiological voltage and potassium concentration.
Ceccarini L. +3 more
openaire +5 more sources
Isocitrate Dehydrogenase Mutations in Cancer: From Bench to Bedside Applications
Mutant isocitrate dehydrogenase affects multiple cancer types. Alterations in IDH1 and IDH2 result in abnormal enzyme activity, leading to the overproduction of D‐2‐hydroxyglutarate (D‐2HG). This metabolite disrupts cellular metabolism and epigenetic regulation, driving cancer initiation, progression, and metastasis.
Yuhan Fang +6 more
wiley +1 more source
Background: The human ether-a-go-go-related gene (HERG) encodes the α-subunit of rapidly activating delayed-rectifier potassium channels. Mutations in this gene cause long QT syndrome type 2 (LQT2).
Takehito Kondo +21 more
doaj +1 more source
Opening closed inward rectifier potassium channel doors
Inwardly rectifying potassium (KIR) channels are essential regulators of membrane potential in excitable and non‐excitable tissues. Although KIR channels exhibit a biophysical preference for potassium influx due to voltage‐dependent block of outward current by polyamines and Mg2+, under physiological conditions, they predominantly mediate K+ efflux ...
Anna Stary‐Weinzinger +3 more
wiley +1 more source

