Of note, detailed time-course analysis demonstrated that the depletion of the MMP clearly preceded cell death and was therefore not a consequence of it (Supplementary Fig S4E).
GCase activity was unaffected in the amygdala of Alzheimer disease patients, suggesting that the deficiency seen in the SN of sporadic PD brains was not simply a consequence of neurodegeneration (Supplementary Fig 2).
This was not a consequence of cell death (supplementary material Fig. S5).
Our class comparison analyses revealed a novel target gene (TSHZ1) in the cVIS6 locus, which was sevenfold upregulated as a consequence of virus integration (Supplementary Figure S2, arrow), but in this cell line, global gene expression was only minimally changed.
The observed differences in CHK2 phosphorylation between HeLa and U2OS cells appeared to be linked to higher basal levels of CHK2, which appeared slightly phosphorylated as a consequence of USP1 depletion (Supplementary Material, Fig. S1C).
While fenofibrate treatment significantly reduced the mRNA expression of TNF-α, no differences in splenic mRNA expression of IL-6, IL-12p40, PHOX-p47, IL-23p19, IL-17, and IFN-γ were observed as a consequence of fenofibrate supplementation (Supplementary Fig S1).
Within several of the terminal taxa in our analysis, we recognized members with approximately twice the number of chromosomes as the mode for that family, and these may also be a consequence of more recent WGDs (supplementary table, Supplementary Material online).
For example, volatile sulphur-containing metabolites such as dimethyl disulphide, methanethiol, dimethyl trisulphide and methoxythiophene, which are generated in humans by the incomplete metabolism of methionine in the transamination pathway, were dramatically downregulated as a consequence of neoplastic cell presence (Supplementary Table 1).
Importantly, hGCN5 depletion did not result in DNA damage as assessed by γH2AX formation, suggesting that the observed decreases in H3K9Ac and H3K56Ac were specific and were not caused indirectly as a consequence of DNA-damage induction (Supplementary Figures 8C and 10).
