Calcium release from the endoplasmic reticulum through the IP₃ receptor ion channel is strongly regulated by a calcium-binding protein in the lumen of the endoplasmic reticulum.

Biochemically detailed modelling of pathways leading to post-synaptic plasticity reveals the dependence of neocortical LTP/LTD on the availability of different proteins and stimulation patterns.

Biochemical analysis reveals molecular mechanisms underlying the activation of the mitochondrial Ca²⁺ uniporter by intracellular Ca²⁺ signals.

Research into light-gated ion channels called channelrhodospins laid the foundations for the development of optogenetics, a technique that has gone on to revolutionize neuroscience.

In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal.

The feedback inhibition of T-type calcium channels by intracellular calcium provides new avenues to better decipher the roles of these low-voltage-activated channels in the fine control of calcium signaling events in physiology and pathophysiology.

A native calcium ion channel has been identified in bacteria for the first time.

Longitudinal imaging of synapses in the brain shows that sensory deprivation differentially modifies specific synapses within individual neurons across distinct layers of the sensory cortex.

A key transcription-factor for osteogenic differentiation, PLZF, acts as a transcriptional activator by binding to active developmental enhancers and facilitates mediator recruitment, but is not involved in enhancer looping.

A multi-species chemical screening platform reveals a conserved role for p38 inhibition in modulating ryanodine receptor-related phenotypes and is adaptable to a range of neuromuscular disorders.