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Flow stimulates PC-1/PC-2 clusters in the plasma membrane of endothelial cells, leading to Ca²⁺ influx, NOS, SK channel, and IK channel activation, vasodilation, and a reduction in blood pressure.

Developmental genetics of sea anemone mechanosensory neurons provides insights into the deep evolutionary history of mechanoreceptor development in animals.

Expansion microscopy combined with light-sheet and STED microscopy elucidated the spatial organization and subcellular composition of two distinct GABAergic CSF-c neuronal subtypes in the lamprey spinal cord.

Genetic analysis identifies the origins of midface defects in mouse models of ciliopathies, revealing a role for ciliary Hedgehog signaling in cell survival.

Disposal of ciliary proteins via ectosomes budding from cilia tip or cilia base acts as a safeguard mechanism when cilia trafficking functions are impaired.

An anchored phosphatase-deacetylase complex participates in primary cilia development.

A transient receptor channel in Toxoplasma gondii that conducts calcium represents the first molecular element that initiates upstream calcium signals that activate parasite pathogenic pathways.

Soluble fragments cleaved from the N-terminus of PC-1 activate the PC-1/PC-2 heteromeric polycystin channel, describing for the first time that the N-terminus itself is an endogenous ligand.

PKD2 (polycystin-2) channels are a major component of a flow-sensing signaling mechanism in endothelial cells that stimulates vasodilation and reduces blood pressure.