Abstract

Seek a cell anchorage galectin bridge: Transforming the wildtype Galectin (Gal)-1 and -3 to a tandem-repeat type variant via rational protein engineering enhanced cis-binding activity with O-Mannosylated core M1 glycopeptides of α-dystroglycan (DG). Furthermore, the Gal-1 variants (but not Gal-3 variants) demonstrated trans-bridging activity with the prepared α-DG core-M1 glycoconjugates and laminins in situ via the carbohydrate-protein interactions. Thus, Gal-1 and its variants are exciting candidates for treating several forms of muscular dystrophy. More information can be found in the Research Article by H. Kaltner, H. Hinou, et al.

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