Tsc2 inactivation in mouse mesenchymal progenitors produced tumors with vascular anomalies reminiscent of human angiomyolipomas, and a gene expression signature in Tsc2-deficient tissues which included Lgals3, as a novel potential biomarker for TSC1/2 loss.

The secreted sugar-binding protein galectin-8 causes osteoblasts to secrete factors that promote the differentiation of bone marrow cells into osteoclasts; targeting this protein could therefore potentially help treat diseases associated with excessive bone loss.

Structurally dissimilar N-glycans can be functionally equivalent, and are produced via a self-correcting feature of the Golgi.

Galectin-9 directly binds to arabinogalactan (AG), leading to the identification of AG-specific monoclonal antibodies that effectively inhibit Mycobacterium tuberculosis growth, providing insights for novel tuberculosis therapies.

Metabolic switches between oxidative phosphorylation and aerobic glycolysis plus glutaminolysis direct T cell function by altering the flux of glucose and glutamine to N-glycosylation.

Galectin-9-deficient mice develop spontaneous autoimmunity, driven by a decreased threshold of B cell activation and enhanced auto-antigen delivery to the spleen by increased B1a-derived autoantibodies.

Protein changes in cerebral cortex following a mild traumatic brain injury (mTBI) identified herein will help in the development of monitoring and response biomarkers that may translate to clinical mTBI.

Protein crystallization is a rare event yet Ym1 crystals made from a chitinase-like protein are abundantly found in eosinophilic airway inflammation, where they promote type 2 immunity.

Adult microglia are born by the division of single surviving microglia that rapidly acquire mature morphologies and functions in order to perform their physiological roles in the brain.

Cellular immunity against Toxoplasma parasites is orchestrated by GBP complexes attacking the parasite membrane.