Proteins of the reticulon and REEP families, homologous to the products of human Hereditary Spastic Paraplegia disease genes, contribute to shaping and continuity of the axonal endoplasmic reticulum network in Drosophila.

The secretory and recycling components of neuronal dendrites, smooth endoplasmic reticulum and endosomes, were discovered to support synaptogenesis underlying a cellular mechanism of learning and memory in the developing brain.

STIM1 regulates the contractility of blood vessels and blood pressure by organizing membrane contact sites and ion channel activity in vascular smooth muscle cells in a manner that is independent of its canonical function in store-operated Ca²⁺entry.

IL-33 plays an important role in the initiation of labor by leading to stress of the ER via an influx of calcium ions in human uterine smooth muscle cells.

The viscous hydraulics of contracting endoplasmic reticulum networks challenge common solute transport theories, suggesting the contraction of peripheral sheets as a plausible driving mechanism.

Purinergic signaling controls mammalian sperm transport.

A new pathway is described involving the estrogen receptor alpha in the acute response of small arteries to flow independent of the ligand (estrogen) and of the nuclear signaling.

Developmental specialization of vomeronasal sensory neurons involves selective upregulation of endoplasmic reticulum genes in a subset of neurons along with a hypertrophic gyroid membrane architecture.

One minute biotinylation with APEX2 peroxidase in living cells identifies established and new components of mitochondrial and ER membranes; dataset intersection and overexpression screen identifies SYNJ2BP overexpression as inducing mitochondria-rough ER contacts.

The protein STIM1 helps to maintain membrane coupling sites in smooth muscle cells that regulate arterial contractility and blood pressure.