Retracted. STAT-1 facilitates the ATM activated checkpoint pathway following DNA damage

Townsend, Paul A., Cragg, Mark S., Davidson, Sean M., McCormick, James, Barry, Sean, Lawrence, Kevin M., Knight, Richard A., Hubank, Michael, Chen, Phang-Lang, Latchman, David S. and Stephanou, Anastasis (2005) Retracted. STAT-1 facilitates the ATM activated checkpoint pathway following DNA damage. Journal of Cell Science, 118 (8), 1629-1639. (doi:10.1242/jcs.01728).

Abstract

In 2015 the following retraction was published in Journal of Cell Science 2015 128: 1064 doi: 10.1242/jcs.169243

We were recently made aware of errors in our paper, which include misrepresentation of western blot data in Figs 4, 5 and 6 as detailed below. The misuse and re-use of western blot bands breaches the editorial policy of Journal of Cell Science, and so we must retract this article. The corresponding author, A.S., regrets the inappropriate figure manipulations of which the co-authors were completely unaware. We deeply regret that the majority of sound research presented in the rest of the paper has been invalidated in this manner, and the concern this will cause to the research community. The co-authors are repeating the affected experiments to determine whether the overall conclusions of the paper remain valid.
1. Fig. 4A, Panel B MDC1 Input lane and Panel A p53BP1 Input lane are the same (flipped horizontally).
2. Fig. 5A (pNBS1), Fig. 5B ATM and Fig. 5G (p53) blots are the same.
3. Fig. 5A (Chk2), Fig. 5C (pChk2) and Fig. 5G (Chk2) blots are the same.
4. Fig. 5B actin and Fig. 5E actin blots are the same.
5. Fig. 6A ATM and pChk2 are the same blot.
6. Fig. 6C and Fig. 6E actin blots are the same.


Original Abstract:
STAT-1 plays a role in mediating stress responses to various stimuli and has also been implied to be a tumour suppressor. Here, we report that STAT-1-deficient cells have defects both in intra-S-phase and G2-M checkpoints in response to DNA damage. Interestingly, STAT-1-deficient cells showed reduced Chk2 phosphorylation on threonine 68 (Chk2-T68) following DNA damage, suggesting that STAT-1 might function in the ATM-Chk2 pathway. Moreover, the defects in Chk2-T68 phosphorylation in STAT-1-deficient cells also correlated with reduced degradation of Cdc25A compared with STAT-1-expressing cells after DNA damage. We also show that STAT-1 is required for ATM-dependent phosphorylation of NBS1 and p53 but not for BRCA1 or H2AX phosphorylation following DNA damage. Expression levels of BRCT mediator/adaptor proteins MDC1 and 53BP1, which are required for ATM-mediated pathways, are reduced in cells lacking STAT-1. Enforced expression of MDC1 into STAT-1-deficient cells restored ATM-mediated phosphorylation of downstream substrates. These results imply that STAT-1 plays a crucial role in the DNA-damage-response by regulating the expression of 53BP1 and MDC1, factors known to be important for mediating ATM-dependent checkpoint pathways.

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Contributors

Author: Mark S. Cragg

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