Experiments in mice have shown than an enzyme that repairs broken DNA inside the nucleus also has a central role in the innate immune system because it is able to detect foreign DNA outside the nucleus.

Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

A newly characterized calcium-activated chloride channel has been implicated in the immune system of Drosophila, shedding light on an enigmatic family of transmembrane proteins that are ubiquitous in nature.

A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

The identification of four acidic amino acids as potential calcium-binding residues in the TMEM16A calcium-activated chloride channel furthers the molecular understanding of this ion channel family.

Post-phosphoryl modification of α-dystroglycan requires the glucuronyltransferase B4GAT1; this enzyme synthesizes the acceptor glycan that serves as a primer for the glycosyltransferase LARGE to synthesize the laminin-binding glycan.

A functional link between representative family members of the CLCA channel regulator family and TMEM16 channels suggests that these protein families may cooperate in influencing multiple homeostatic and disease physiologies.

In mice, cyclic di-GMP is an effective mucosal pneumococcal vaccine adjuvant that stimulates the immune response via two distinct mechanisms.

A comprehensive analysis of the human MICOS complex has identified a novel subunit called QIL1 that is required for cristae junction formation in human cells and Drosophila, through its role in the assembly of the MICOS complex.

The amino acids that are necessary for phospholipid scrambling by ANO6/TMEM16F can, via domain swapping, confer scrambling activity to the chloride ion channel ANO1 that normally does not scramble phospholipids.