Crystal structures of the mouse CMP-sialic acid transporter in complex with both CMP and CMP-sialic acid reveal the mechanisms of substrate selectivity and transport.

Glycans are remodeled by HIV and are determinants of CD4+ T cell susceptibility to HIV infection.

Neuronal activity triggers the dispersal of the Golgi into dendritic Golgi satellites, leading to reshaping of the neuronal surface glycoproteome through processing of glycans to mature, sialic acid-containing forms.

By distributing receptor-binding and receptor-destroying proteins asymmetrically on their surface, filamentous influenza A virus particles create a Brownian ratchet that facilitates their passage through mucus.

Sialoside-based pattern recognition by Siglecs directly regulates toll-like receptor signaling and a sialidase inhibitor protects against endotoxemia.

By contributing to the maintenance of ROS homeostasis, CD33-related Siglecs control oxidative damage and influence rate of aging and lifespan.

Cholera intoxication of human colonic epithelial cells is dependent on recognition of protein glycosylation and fucosylation, not exclusively on ganglioside recognition as proposed previously.

Structure of the dimeric Haemophilus influenzae TRAP transporter (SiaQM) reveals two Na⁺ sites, the substrate-binding site and lipid-binding sites, and weak but promiscuous binding of SiaP to SiaQM.

The sialylation pathway is uniquely partitioned in Drosophila between glia and neurons and mediates a novel mechanism of glia-neuron coupling that regulates neural functions, promotes tolerance to heat and oxidative stress, and maintains the normal level of voltage-gated sodium channels.

Ggta1 deletion in mice shapes and reduces the microbiota pathogenicity and probably contributed to the natural selection of GGTA1 loss-of-function mutations in the ancestral primates that gave rise to humans.