After this article [1] was published, concerns were raised about results presented in Figs 3, 4, 6, and 7. Specifically:
- The following panels appear similar:
- ○ The Fig 3A Bak, Bax and ꞵ-actin panels of this article [1] and the Fig 3A Bak, Bax and ꞵ-actin panels of [2].
- ○ The Fig 6A Mel-2a VDAC panel and the Fig 6A A357-Bcl-2 VDAC panel.
- ○ The Fig 6A A375 Mock Bcl-xAK panel and the Fig 6A A375 Bcl-2 Bcl-xAK panel.
- ○ The Fig 6B Mel-2a Bak panel and the Fig 6B A357-Bcl-2 VDAC panel when flipped vertically.
- ○ The Fig 7A Bcl-2 panel of this article [1] and the Fig 5A Bcl-2 panel of [2] despite being used to represent results obtained from different cell lines.
- The Fig 4A Control DU145 Bax-EGFP and Bcl-xAK OFF DU145 Bax-EGFP panels appear to partially overlap.
The corresponding author responded to queries about the above, stating that they were unable to provide the raw data. In the absence of the raw data the issues with these figures cannot be resolved.
In light of the above concerns which question the reliability of the published results, the PLOS ONE Editors retract this article.
JE agreed with the retraction. MP, AMH, BG, PTD, and ES either did not respond directly or could not be reached.
References
- 1. Plötz M, Hossini AM, Gillissen B, Daniel PT, Stockfleth E, Eberle J (2012) Mutual Regulation of Bcl-2 Proteins Independent of the BH3 Domain as Shown by the BH3-Lacking Protein Bcl-xAK. PLoS ONE 7(4): e34549. pmid:22506026
- 2. Plötz M., Gillissen B., Hossini A, Daniel PT, Eberle J (2012) Disruption of the VDAC2–Bak interaction by Bcl-xS mediates efficient induction of apoptosis in melanoma cells. Cell Death Differ 19, 1928–1938. pmid:22705850
Citation: The PLOS ONE Editors (2024) Retraction: Mutual Regulation of Bcl-2 Proteins Independent of the BH3 Domain as Shown by the BH3-Lacking Protein Bcl-xAK. PLoS ONE 19(11): e0314638. https://doi.org/10.1371/journal.pone.0314638
Published: November 22, 2024
Copyright: © 2024 The PLOS ONE Editors. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.