UseCases_ArguminSci_Discourse  

PubMed:11494364 JSONTXT 8 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 0-121 DRI_Outcome denotes Age-dependent and tissue-specific CAG repeat instability occurs in mouse knock-in for a mutant Huntington's disease gene.
T2 122-251 DRI_Challenge denotes Huntington's disease (HD) is a neurodegenerative disorder characterized by the expansion of CAG repeats in exon 1 of the HD gene.
T3 252-442 DRI_Outcome denotes To clarify the instability of expanded CAG repeats in HD patients, an HD model mouse has been generated by gene replacement with human exon 1 of the HD gene with expansion to 77 CAG repeats.
T4 443-574 DRI_Background denotes Chimeric proteins composed of human mutated exon 1 and mouse huntingtin are expressed ubiquitously in brain and peripheral tissues.
T5 575-744 DRI_Outcome denotes One or two CAG repeat expansion was found in litters from paternal transmission, whereas contraction of CAG repeat in litters was observed through maternal transmission.
T6 745-879 DRI_Outcome denotes Elderly mice show greater CAG repeat instability than younger mice, and a unique case was observed of an expanded 97 CAG repeat mouse.
T7 880-1026 DRI_Challenge denotes Somatic CAG repeat instability is particularly pronounced in the liver, kidney, stomach, and brain but not in the cerebellum of 100-week-old mice.
T8 1027-1163 DRI_Outcome denotes The same results of expanded CAG repeat instability as observed in this HD model mouse were confirmed in the human brain of HD patients.
T9 1164-1401 DRI_Background denotes Glial fibrillary acidic protein (GFAP)-positive cells have been found to be increased in the substantia nigra (SN), globus pallidus (GP), and striatum (St) in the brains of 40-week-old affected mice, although without neuronal cell death.
T10 1402-1535 DRI_Outcome denotes The CAG repeat instability and increase in GFAP-positive cells in this mouse model appear to mirror the abnormalities in HD patients.
T11 1536-1666 DRI_Outcome denotes The HD model mouse may therefore have advantages for investigations of molecular mechanisms underlying instability of CAG repeats.