7XXW

Macaca fascicularis galectin-10/Charcot-Leyden crystal protein with glycerol

Summary for 7XXW

• Entry DOI: 10.2210/pdb7xxw/pdb
• Descriptor: Galectin, GLYCEROL (3 entities in total)
• Functional Keywords: macaca fascicularis galectin-10/charcot-leyden crystal protein with glycerol, sugar binding protein
• Biological source: Macaca fascicularis (crab-eating macaque)
• Total number of polymer chains: 1
• Total formula weight: 16290.41

Authors

Su, J.Y. (deposition date: 2022-05-31, release date: 2023-04-12, Last modification date: 2023-11-29)

Primary citation

Na, H.,Sayed, H.,Ayala, G.J.,Wang, X.,Liu, Y.,Yu, J.,Liu, T.,Mayo, K.H.,Su, J.
Glutathione disrupts galectin-10 Charcot-Leyden crystal formation to possibly ameliorate eosinophil-based diseases such as asthma.
Acta Biochim.Biophys.Sin., 55:613-622, 2023

PubMed Abstract: Charcot-Leyden crystals (CLCs) are the hallmark of many eosinophilic-based diseases, such as asthma. Here, we report that reduced glutathione (GSH) disrupts CLCs and inhibits crystallization of human galectin-10 (Gal-10). GSH has no effect on CLCs from monkeys ( or ), even though monkey Gal-10s contain Cys29 and Cys32. Interestingly, human Gal-10 contains another cysteine residue (Cys57). Because GSH cannot disrupt CLCs formed by the human Gal-10 variant C57A or inhibit its crystallization, the effects of GSH on human Gal-10 or CLCs most likely occur by chemical modification of Cys57. We further report the crystal structures of Gal-10 from . and . , along with their ability to bind to lactose and inhibit erythrocyte agglutination. Structural comparison with human Gal-10 shows that Cys57 and Gln75 within the ligand binding site are responsible for the loss of lactose binding. Pull-down experiments and mass spectrometry show that human Gal-10 interacts with tubulin α-1B, with GSH, GTP and Mg stabilizing this interaction and colchicine inhibiting it. Overall, this study enhances our understanding of Gal-10 function and CLC formation and suggests that GSH may be used as a pharmaceutical agent to ameliorate CLC-induced diseases.

PubMed: 36988350
DOI: 10.3724/abbs.2023050

Experimental method

X-RAY DIFFRACTION (1.63 Å)