UseCases_ArguminSci_Discourse  

PubMed:24725412 JSONTXT 24 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 0-94 DRI_Challenge denotes Ribosomal protein s15 phosphorylation mediates LRRK2 neurodegeneration in Parkinson's disease.
T2 95-214 DRI_Approach denotes Mutations in leucine-rich repeat kinase 2 (LRRK2) are a common cause of familial and sporadic Parkinson's disease (PD).
T3 215-375 DRI_Background denotes Elevated LRRK2 kinase activity and neurodegeneration are linked, but the phosphosubstrate that connects LRRK2 kinase activity to neurodegeneration is not known.
T4 376-494 DRI_Outcome denotes Here, we show that ribosomal protein s15 is a key pathogenic LRRK2 substrate in Drosophila and human neuron PD models.
T5 495-639 DRI_Outcome denotes Phosphodeficient s15 carrying a threonine 136 to alanine substitution rescues dopamine neuron degeneration and age-related locomotor deficits in
T6 640-652 Token_Label.OUTSIDE denotes G2019S LRRK2
T7 653-700 DRI_Outcome denotes transgenic Drosophila and substantially reduces
T8 701-722 Token_Label.OUTSIDE denotes G2019S LRRK2-mediated
T9 723-790 DRI_Outcome denotes neurite loss and cell death in human dopamine and cortical neurons.
T10 791-976 DRI_Outcome denotes Remarkably, pathogenic LRRK2 stimulates both cap-dependent and cap-independent mRNA translation and induces a bulk increase in protein synthesis in Drosophila, which can be prevented by
T11 977-999 Token_Label.OUTSIDE denotes phosphodeficient T136A
T12 1000-1004 DRI_Outcome denotes s15.
T13 1005-1143 DRI_Background denotes These results reveal a novel mechanism of PD pathogenesis linked to elevated LRRK2 kinase activity and aberrant protein synthesis in vivo.