Phosphorylation of a highly conserved serine residue is a physiological response of Escerichia coli to environmental potassium levels that inhibits transport by KdpFABC to maintain cellular homeostasis.
Loss of potassium channel activity from fast-spiking interneurons increases their excitability leading to unexpectedly increased fast excitatory transmission and seizure susceptibility.
A mouse model of human muscle myopathy is used to provide mechanistic insight, identify possible biomarkers of disease, and suggest possible therapeutic strategies to alleviate muscle weakness.
An inducedpluripotent stem cell (iPSC)-based model of KCNQ2-associated developmental epileptic encephalopathy suggests that disease is driven by dyshomeostaic neuronal mechanisms that are downstream of loss of M-current.
The SCHENGEN3 protein is needed for the progression of isolated microdomains into a continuous band, which is necessary for the establishment of the major extracellular diffusion barrier in plant roots: the Casparian strip.
Mathematical models with experimental validation show that chloride transporters in the cell membrane, and not negatively charged impermeant molecules, generate the driving force used by GABA receptors to silence neurons.
Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.
As in humans, Drosophila hearts are able to maintain contractile performance during healthy aging, but this maintenance is associated with an increased susceptibility to progressive dysrhythmias that can lead to fibrillatory arrest.
Contrary to a long-standing hypothesis, the neuronal death that leads to muscle wastage in amyotrophic lateral sclerosis does not result from overactivity of those neurons during development.
