Researchers at Kyoto University have discovered a genetic mutation that causes lethal arrhythmia in humans. The study found that a novel variant of the CALM2 gene produces robust arrhythmogenicity in human-induced pluripotent stem cell-derived cardiomyocytes.
SourceKyoto University·JournalCirculation Arrhythmia and Electrophysiology·TypeExperimental study·DateApr 13, 2023
Researchers at Osaka University discovered that mutant variants of the RyR1 calcium channel protein are more sensitive to heat than normal proteins, leading to a cycle of activation that can cause malignant hyperthermia. This finding provides new insight into the condition and could lead to preventive and treatment strategies.
SourceOsaka University·JournalProceedings of the National Academy of Sciences·TypeExperimental study·DateAug 8, 2022
Scientists at Columbia University's Zuckerman Institute have discovered that floods of calcium originating from within neurons can boost learning and recall. The finding sheds light on the mechanisms underlying learning and memory, potentially providing new insights into Alzheimer's disease.
SourceColumbia University·JournalScience·TypeExperimental study·DateMar 17, 2022
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Atrial fibrillation is a major concern due to its association with serious complications like heart failure and stroke. Researchers have identified a new piece of the puzzle that has changed the field's understanding of the molecular mechanisms leading to atrial fibrillation, involving a phosphatase regulatory subunit known as PPP1R3A.
SourceBaylor College of Medicine·JournalCirculation·DateAug 20, 2019
Scientists discovered how mutations in the IP3R1 protein contribute to degenerative movements disorders like spinocerebellar ataxias. By disrupting calcium release, these mutations impair motor control and lead to cerebellum dysfunction.
SourceRIKEN·JournalProceedings of the National Academy of Sciences·DateNov 12, 2018
A team of researchers used a multidisciplinary approach to study the effects of heart failure on electrical activity and calcium release in heart cells. They found increased variability in Ca2+ transient kinetics, indicating an uncoupling between membrane depolarization and Ca2+-release.
A new study reveals that Cav1.3 calcium channels play a critical role in controlling the ticking of pacemaker cells in the sinoatrial node, which regulates heart rate. The absence of these channels leads to reduced frequency of Ca2+ transients and bradycardia in mice.
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Mutations in RYR1 lead to calcium release channel dysfunction, causing dominant-negative effect that reduces muscle force generation. The study provides a comprehensive analysis of the consequences of this mutation in muscle fibers.
SourceRockefeller University Press·JournalJournal of General Physiology·DateDec 13, 2010
Research shows prolonged stress can induce cell death in aging-related diseases like atherosclerosis and neurodegeneration by triggering the endoplasmic reticulum (ER) to release calcium stores. ER proteins ERO1-alpha and IP3R play a crucial role in this process, suggesting potential new targets for treatment.
SourceRockefeller University Press·JournalJournal of Cell Biology·DateSep 14, 2009
UT Southwestern researchers have discovered a connection between disrupted calcium metabolism in nerve cells and a fatal genetic neurological disorder called spinocerebellar ataxia 3. The study suggests that blocking excessive calcium release may alleviate symptoms, with results showing improved coordination and slowed brain atrophy in...
Researchers have made a breakthrough in unravelling the causes of sudden cardiac death in young people, linking it to genetic mutations in calcium release channels. These mutations destroy the channels' ability to work properly after stress or exercise, leading to fatal heart rhythms.
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