Xingli Li

This study shows NLK disrupts nuclear import, causing TDP43 mislocalization in ALS, and suggests NLK as a therapeutic target.

This study investigates the role of stress granule formation in neurodegeneration, finding that reducing stress granules exacerbates disease phenotypes in models of ataxia, ALS, and FTD.

This study identifies TDP43 autoregulation as a source of shortened isoforms, showing they are regulated by NMD and post-translational degradation, and their dysregulation leads to neurodegeneration.

The paper develops NMDq, a next-generation sequencing method to quantify NMD status, and applies it to ALS and FTD, finding no significant PTC differences but showing UPF1 regulates RNA homeostasis through alternative polyadenylation.

This study shows that RNA methylation influences TDP43 binding and contributes to neurodegeneration in ALS by modulating RNA stability and TDP43 function.

This study shows that neuronal activity regulates MATR3 levels and function through calpain cleavage and Ca2+/calmodulin binding, linking these processes to ALS pathology.

This study shows that inhibiting GSK3 reduces TDP-43 levels and neurotoxicity in mammalian neurons by promoting TDP-43 turnover through a caspase-dependent mechanism.