Fig. 7: Facilitation of mitochondrial energy generation by AK2 limits MYC-induced apoptosis.
From: MYC sensitises cells to apoptosis by driving energetic demand

A Schematic of the nucleotide environment in the mitochondrial intermembrane space where AK2 is located. B Induction of AK2 expression by MYC shown by qRT-PCR (left panel) and western blot (right panel). Statistical analysis was carried out on n = 3 replicates using an unpaired two-tailed t test. C Ratio of peak intensities of ATP/AMP of MYC cells with knockdown of AK2 as measured by LC-MS. An ordinary one-way ANOVA was used to determine statistical significance (n = 3 biological replicates). D, E AnnexinV/PI assays in MRC-5 cells with (D) siRNA-mediated knockdown and (E) overexpression of AK2. An ordinary one-way ANOVA was used to determine statistical significance (n = 3 biological replicates). F Co-expression analysis (mean-centred log2 intensity) of MYC versus nucleotide biosynthesis and AK2 genes derived from Affymetrix array data from 2999 breast cancers. The genes in bold are highly significant (P < 0.00001). Paired boxplots show the distributions of expression for each gene between two groups of microarray profiled breast tumours, MYC high and MYC low, based upon lower and upper tertiles of MYC expression (see 'Methods'). In each boxplot, the central point depicts the median value, the box bounds span Q1 to Q3, and left and right whiskers show Q1 − 1.5*IQR and Q3 + 1.5*IQR, respectively. For all statistical tests, P ≤ 0.05 was considered significant, and error bars show the standard error of the mean.