Here, we report that GlyRS mutants interact aberrantly with HDAC6 and stimulate its deacetylase activity on tubulin.
[from the second reference]:As was previously reported in mouse cells,[9] immunoblot analysis quantifying GARS in HDAC6 immuno-precipitates confirmed that GARS1P234KY exhibits aberrant interaction between GARS and HDAC6 proteins in cultured spinal neurons; a phenomenon not observed in wild-type controls.