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. 2003 Sep 1;22(17):4577. doi: 10.1093/emboj/cdg454

Corrigenda

PMCID: PMC202383

The oncogenic RAS2val19 mutation locks respiration, independently of PKA, in amode prone to generate ROS. Hlavatá Lydie, Aguilaniu Hugo, Pichová Alena, Nyström Thomas. The EMBO Journal. 2003;22:3337–3345. doi: 10.1093/emboj/cdg314.

We have repeated all the respiration experiments in the above paper with lower concentrations of TET and CCCP (20–100 µM TET and 1–5 µM CCCP) since the concentrations originally used may potentially cause non-specific effects. Using the lower range of TET and CCCP concentrations, we find that the respiratory state value (RSV) differences are still significant (10.65 in the RAS2val19 cells against 69.61 in wild-type cells). Thus, the conclusions of the paper remain unchanged. Nonetheless, the distinction should be made that the RAS2val19 mutant shows a respiration closer to state 4 than the wild type but is not completely non-phosphorylating. The corrected RSV table (Table I) is as follows:

Table I. Basal respiration rates and RSVs of different strains.

Strain Respiratory characteristics
  Basal rate (µM O2/min) RSV
wt 13.36 ± 2.02 69.61 ± 3.9
RAS2val19 4.49 ± 1.03 10.65 ± 4.45
wt + Yep13 14.61 ± 1.40 34.81 ± 2.7
RAS2val19 + Yep13 7.85 ± 0.57 9.35 ± 5.6
wt + Pde2p 23.27 ± 3.66 42.47 ± 2.8
RAS2val19 + Pde2p 13.76 ± 3.99 6.16 ± 10
wt + Yepd 17.80 ± 1.59 51.49 ± 4.76
RAS2val19 + Yepd 3.16 ± 1.26 15 ± 2.89
wt + UCP1 18.15 ± 6.62 22.59 ± 1.49
RAS2val19 + UCP1 14.61 ± 1.40 53.67 ± 9.56
bcy1-13 3.09 ± 1.23 44.23 ± 2.1

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