A structural and functional analysis of the electron transfer complex between a sulfite oxidase and its redox protein partner reveals an elegant compromise between the requirements for fast and efficient electron transfer and reaction specificity.

Structures of CysZ show a antiparallel membrane protein with an unanticipated fold and together with functional characterization provide insight into a bacterial sulfate translocating system.

Heparan Sulfate Proteoglycans function as receptors for the R-spondins, a family of growth factors that amplify the strength of WNT signaling during development and in adult stem cells.

Indoxyl sulfate, a key uremic toxin in chronic kidney disease (CKD), induces trained immunity in monocytes via crosstalk between aryl hydrocarbon receptor (AhR)-dependent epigenetic reprogramming by enhancement of the arachidonic acid pathway and AhR-independent metabolic rewiring.

A potentially useful cyanobacterial sulfated exopolysaccharide and its biosynthesis and regulation genes, which contribute to the laboratorial bloom formation, are elucidated for the first time among prokaryotes.

4,6-Sulfation of chondroitin sulfate proteoglycans prevents sympathetic nerve regeneration into the infarct after myocardial ischemia/reperfusion, and reducing this sulfation promotes nerve regeneration and decreases arrhythmia susceptibility.

Heparan sulfates in the vessel wall bind and regulate signaling from the megakaryocyte/platelet-specific inhibitory receptor G6b-B, a critical regulator of platelet homeostasis.

Heparan sulfate synthesis by mature oligodendrocytes creates a protective and permissive environment controling microglia and oligodendrocyte progenitors reactivation during remyelination.

A novel dimethylsulfoniopropionate lyase was identified, which catalyzes dimethyl sulfide releasing by a new mechanism and is found in several bacterial lineages, revealing its important roles in global sulfur cycling.

Heparan sulfate-RAGE interaction is essential for normal function of RAGE in osteoclastogenesis and drug-induced liver damage, which can be targeted to curb RAGE activation as a new opportunity.