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.

β-adrenergic receptors at the Golgi apparatus activate a local signaling pathway, not accessed by cell surface receptors, to drive cardiac hypertrophy and could represent a target for heart failure therapy.

Genetics, in vivo imaging, and unbiased chemical biology screens reveal that Trpv6 functions as a cellular quiescence regulator and delineates a Trpv6-mediated Ca²⁺ signaling pathway maintaining the quiescent state.

The substrate for evolutionary divergence does not lie in changes in neuronal cell number or targeting, but rather in sensory perception and synaptic partner choice within invariant, prepatterned neuronal processes.

Shortage of blood-borne apolipoprotein-M–bound sphingosine-1-phosphate, which accompanies various brain disorders, causes paracellular leak and increase in transcytosis at the blood–brain barrier, which can be reversed, thus is of clinical relevance.

An unbiased RNAseq based strategy to identify targetable pathways and a streamlined lentiviral system provide a state of the art advance on direct fibroblast to neuron conversion.