Figure 6: ERAD inhibition and ER stress triggered by Htt96Q can be compensated by overexpression of p97/VCP. | Nature Communications

Figure 6: ERAD inhibition and ER stress triggered by Htt96Q can be compensated by overexpression of p97/VCP.

From: Soluble forms of polyQ-expanded huntingtin rather than large aggregates cause endoplasmic reticulum stress

Figure 6

(a) Induction of eIF2α phosphorylation after 24 h of Htt96Q expression is strongly inhibited by coexpression of p97/VCP. (*P-value=0.02, Student’s t-test (unpaired, two-tailed)). (b) Accumulation of H2a caused by Htt96Q expression is strongly reduced by coexpression of p97/VCP. P97/VCP has only a minor, non-significant effect in reducing the Htt96Q fraction in insoluble aggregates. Values were corrected by the anti-β-tubulin signal as a loading control. (**P-value<0.01, ***P-value=0.00006, Student’s t-test (unpaired, two-tailed)). (c) Inhibition of H2a degradation on expression of Htt96Q is cancelled by overexpression of p97/VCP. Experiment similar to that in Fig. 1b but in HEK 293 cells with and without coexpression of p97. The graph shows percent of H2a in the chase relative to pulse (100%). Where indicated, p97 overexpression was done using 6xHis-tagged p97/VCP in all cases. All graphs in this figure are averages of three experiments±s.e.

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