p(MGI:Mapt, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205))

Entity

Name

Mapt

Namespace

mgi

Namespace Version

20181021

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Mice in which the critical autophagy gene Atg7 is knocked out in forebrain neurons develop age-dependent neurodegeneration with accumulation of phosphorylated tau within intracellular inclusions (99). These inclusions specifically contained tau phosphorylated at AT8, AT100, and TG3 epitopes, but not PHF1. Significantly, if tau was also knocked out in these autophagy-deficient mice, neurodegeneration was reduced (99). PubMed:24027553

Immunostaining with AT8 antibody revealed abundant AT8-positive neurons in AAV–Otub1-injected mice, absent in AAV–GFP-infected mice (Fig. 7a), at 2 months postinjection. PubMed:28083634

Biochemical analysis further confirmed increased AT8-positive Tau by Otub1 expression (Fig. 7b), with AT8 phosphorylated Tau more robustly increased than total Tau, as reflected by the AT8/total Tau ratio. PubMed:28083634

Immunostaining and biochemical analysis, 2 months postinjection, unambiguously revealed that the catalytically dead mutant C91A did not affect AT8-stained Tau in vivo, while N-terminal truncated mutant of Otub1 increased AT8-positive Tau in vivo, similarly as wild-type Otub1 (Fig. 8). PubMed:28083634

Immunostaining and biochemical analysis, 2 months postinjection, unambiguously revealed that the catalytically dead mutant C91A did not affect AT8-stained Tau in vivo, while N-terminal truncated mutant of Otub1 increased AT8-positive Tau in vivo, similarly as wild-type Otub1 (Fig. 8). PubMed:28083634

Immunostaining and biochemical analysis, 2 months postinjection, unambiguously revealed that the catalytically dead mutant C91A did not affect AT8-stained Tau in vivo, while N-terminal truncated mutant of Otub1 increased AT8-positive Tau in vivo, similarly as wild-type Otub1 (Fig. 8). PubMed:28083634