ArticleBMC cardiovascular disorders2026
The p.Arg52Leu variant in GNB2 causes a gain-of-function due to an increase of I
Article in BMC cardiovascular disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundInitially discovered and published in 2017, the heterozygous mutation (p.Arg52Leu) in the GNB2 gene is associated with sinus node dysfunction (SND) and atrioventricular block (AVB). Electrophysiological characterization using heterologous expression systems has demonstrated that this R52L GNB2 variant results in a larger G-protein-activated K
methodsHere, we differentiated CMs derived from human induced pluripotent stem cells (hiPSC-CMs) of a patient carrying the pathogenic p.Arg52Leu GNB2 variant (hiPSC
resultsPatch-clamp experiments demonstrated that without GIRK channel stimulation the maximal diastolic potential (MDP) and spontaneous pacing rate did not differ between mutant and control cell lines and, moreover, a constitutively active I
conclusionThe reported, mutant GNB2 in patient-derived CMs is associated with a gain-of function upon GIRK channel stimulation and thereby a larger I CLINICAL TRIAL NUMBER: not applicable.
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