Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

Apoptotic cells release molecules to recruit macrophages, but do not cause inflammation because they also secrete AMP that functions as a ‘calm down’ signal.

There are inherent tradeoffs in the control of cellular response variability by paracrine communication during the establishment of initial wound response signaling gradients.

Astrocytes regulate the pruning of excitatory synapses during early life through ATP signaling.

The endoplasmic reticulum serves as a direct and primary source of calcium ions for the lysosome.

Crystal structures of a mammalian P2X7 receptor and structure-based functional studies reveal a novel drug-binding site and subtype-specific conformational rearrangements required for channel opening.

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.

CO₂/H⁺-dependent purinergic signaling by astrocytes provides specialized control of vascular tone in a brainstem respiratory center in a manner that contributes to respiratory behavior.

Genetic and biochemical analyses demonstrate that cell-surface lectin receptors can potentially function as extracellular NAD⁺-binding receptors and provide direct evidence for extracellular NAD⁺ being a bona fide endogenous signaling molecule in plants.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.