Skip to main content

Advertisement

Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: ULK1-mediated phosphorylation of ATG14 promotes autophagy and is impaired in Huntington’s disease models

Fig. 6

ULK1 activity regulates the degradation of polyQ proteins. a FLAG-ATG14 S29 WT, SA, or SE, Beclin 1-AsRed, and dual myc-Vps34 his-Vps15 plasmid were overexpressed in mCFP-65Q expressing HeLa cells then treated with rapamycin overnight. Cell lysates were separated into soluble and insoluble fractions. PolyQ was measured in the insoluble fraction. b Quantification of polyQ degradation in the insoluble fraction. Degradation was calculated as the ratio of control sample vs. rapamycin sample **p < 0.01 (n = 4). Data are represented as mean +/− SEM. c Myc empty vector, myc-ULK1 WT or KI were overexpressed in mCFP-65Q expressing HeLa cells and cells were lysed 48 h after transfection. Cell lysates were separated into soluble and insoluble fractions. PolyQ was measured in the insoluble fraction. d Quantification of polyQ levels in the insoluble fraction. Values were normalized to empty vector condition. *p < 0.05 n.s. not significant (n = 4). Data are represented as mean +/− SEM

Back to article page