C. elegans EFHC1 influences neuronal transmission through the cilium and the synapse.

Trafficking of optogenetic tools to primary cilia using nanobodies allows to study cAMP signaling with spatial and temporal resolution independent of the cell body.

Outward calcium ion currents desensitize the human PKD2-L1 ion channel via a mechanism that is independent of cytosolic motifs.

Electron tomography and biochemical approaches demonstrate a direct role for WDR35, beyond integrity of the IFT-A holocomplex, in the formation and fusion of electron-dense-coated vesicles to the ciliary sheath and pocket for delivery of cargos necessary for axoneme elongation.

Direct patch clamp of ependymal motile cilia reveals that voltage-gated calcium channels in the cell body dominate their electrical and calcium signaling properties.

L-amino acids are agonists of calcium-sensing receptor, and act jointly with calcium and phosphate ions to control receptor function.

A series of quantitative behavioural and opto-physiological analyses using a novel robot microscope system reveals that C. elegans computes the time-differential and time-integral of sensory information for decision-making during olfactory navigation.

Structure modeling, site-directed mutagenesis, and current recordings revealed the mechanism by which stabilization of voltage sensors in the resting and activated states determines the gating properties of the Ca_V1.1 calcium channel.

Calcium-calcineurin signaling cascade drives the acquisition of both the phenotype of the most self-reactive naive CD4 T cells and their enhanced cell-intrinsic ability to commit into induced regulatory T cells upon activation.

Striatal cholinergic interneurons and astrocytes lose cilia and show dysregulation of Hedgehog signaling in mice with a Parkinson's disease-associated, G2019S LRRK2 mutation or upon loss of PPM1H phosphatase specific for LRRK2-phosphorylated Rab GTPases.