The structure of a pannexin 1 uncovers the extracellular loops of pannexin 1 as important structural motifs for ion selectivity and channel inhibition.

An in silico analysis of gap junction proteins supports the hypothesis that connexins replaced the primordial innexins in chordate gap junctions due to an evolutionary bottleneck.

The innexin protein UNC-7, a homologue of vertebrate pannexins, plays a specific, gap junction-independent role in C. elegans mechanosensation.

A CO₂ receptor and a mechanism for the CO₂-mediated opening of gap junction hemichannels have been identified.

Endothelial pannexin 1-P2Y2 purinergic receptor-TRPV4 channel signaling, facilitated by caveolin-1, is a novel pathway for lowering pulmonary arterial pressure.

Purified Pannexin 1 channels activated by caspase cleavage in proteoliposomes reconstitute a permeation pathway for intercellular signaling molecules important in inflammation and cell clearance.

A novel role of endosomal machineries retromer and ESCRT in membrane delivery of Drosophila septate junction components is required for maintenance of junction integrity and epithelial barrier function.

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

Autocrine activation of macrophages is modulated by Connexin-43-mediated ATP release in response to TLR-4 and -2 agonists in a P2Y1-dependent manner, ultimately determining sepsis survival.

Cryo-EM structures and molecular dynamics simulations of Cx43 gap junction channel and hemichannel reveal a putative closed state.