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.

It is shown that the absence of the centrosome protein ninein provokes premature ossification during mouse development, due to a defect in the fusion of precursor cells into syncytial osteoclasts.

Somatic gonad architecture is regulated by innexin function, but sheath cell position does not determine germ cell exit from the stem cell pool.

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

An inadequate engagement of the inflammation resolution circuit centred on Annexin A1 contributes to the excessive inflammation observed in severe DENV infection, suggesting FPR2/ALX agonists as a therapeutic target for dengue disease.

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.

Cleavage of pannexin-1 channel by caspases facilitates the loss of intracellular ATP level and attenuates glycolytic metabolism of apoptotic cells.