The functional interaction of Na+ and KATP channels at the intercalated disk of cardiomyocytes depends on Ankyrin G and is clinically relevant since KATP channel mutations affect Na+ channel expression.
The newly discovered Titin internal promoter may explain why the severity of dilated cardiomyopathy in patients with truncating mutations in Titin varies dramatically depending on position of the mutation.
Experiments in a mouse model for Alzheimer’s disease using germ-free and conventionally housed animals reveal that microbiota-derived short-chain fatty acids promote the deposition of cerebral Aβ plaques.
Mitochondrial-targeted SS-31 peptide ameliorates mitochondrial dysfunction and rescues pre-existing cardiac dysfunction in old mice, supporting the translational potential of mitochondrial protective interventions to treat age-related diseases.
As the first fully genetically encoded method, PARIS allows cell-specific, long-term, repeated measurements of gap junctional coupling with high spatiotemporal resolution, facilitating its study in both health and disease.