p(HBP:"4R tau", var("p.Lys280del"))

Entity

Name

4R tau

Namespace

HBP

Namespace Version

20190207

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/cf4d8bb88754f036b943b4d94ad96e103dcb7149/export/hbp-names.belns

As expected, we observed a significant impairment of mitochondrial distribution with overexpression of all three tau constructs (p < 0.0001, Wilcoxon test for GFP control versus 4R-tau, GFP versus tauC3, and GFP versus K18ΔK280) (Fig. 5). PubMed:25374103

Taken together, these data indicate that tau-overexpression leads to abnormal mitochondrial trafficking that can be rescued by CHIP-co-expression PubMed:25374103

After cyclohexamide treatment, we could still detect a significant decrease in tau levels in cells that were co-transfected with CHIP indicating that the reduction in tau levels due to CHIP is due to degradation and not to transcriptional down-regulation (Supplementary Fig. 3). PubMed:25374103

Interestingly, a significant decrease in tau levels was seen with the co-transfection of CHIPΔU (U-box deleted) when transfected with either K18ΔK280 or 4R-Tau. PubMed:25374103

Densitometry analysis of total tau levels of H4- cell lysates on SDS-PAGE showed a 2.0 to 2.5 fold lower levels of tau (4R-tau, tauC3, and K18ΔK280) with co-expression with CHIP, respectively (Fig. 1). PubMed:25374103

After cyclohexamide treatment, we could still detect a significant decrease in tau levels in cells that were co-transfected with CHIP indicating that the reduction in tau levels due to CHIP is due to degradation and not to transcriptional down-regulation (Supplementary Fig. 3). PubMed:25374103

Toxicity assays revealed that neither CHIP nor any of the tau constructs caused cell death compared to the control GFP vector (Supplementary Fig. 1). PubMed:25374103

As expected, we observed a significant impairment of mitochondrial distribution with overexpression of all three tau constructs (p < 0.0001, Wilcoxon test for GFP control versus 4R-tau, GFP versus tauC3, and GFP versus K18ΔK280) (Fig. 5). PubMed:25374103

Taken together, these data indicate that tau-overexpression leads to abnormal mitochondrial trafficking that can be rescued by CHIP-co-expression PubMed:25374103