The University of Southampton
University of Southampton Institutional Repository
Warning ePrints Soton is experiencing an issue with some file downloads not being available. We are working hard to fix this. Please bear with us.

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

Retracted. STAT-1 facilitates the ATM activated checkpoint pathway following DNA damage
Retracted. STAT-1 facilitates the ATM activated checkpoint pathway following DNA damage
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.
ATM, cell cycle, Chk2, 53BP1, MDC1, STAT-1
0021-9533
1629-1639
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db
Cragg, Mark S.
ec97f80e-f3c8-49b7-a960-20dff648b78c
Davidson, Sean M.
b8eeed87-5d86-42ca-8844-25bf6887253c
McCormick, James
9f5d47a6-87d4-48c3-a952-4133b710bbb1
Barry, Sean
b65013c6-a911-44ee-a98f-3ff7420cced8
Lawrence, Kevin M.
ff8347b7-930c-4414-beab-65f6d6514b73
Knight, Richard A.
da6172f8-cacc-4330-871a-85dea9e893a4
Hubank, Michael
cd19379f-9a05-4891-9c7c-1f6f24d7a13b
Chen, Phang-Lang
6225ade7-1868-4cd2-a767-d2ca35d6433f
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3
Townsend, Paul A.
a2680443-664e-46d0-b4dd-97456ba810db
Cragg, Mark S.
ec97f80e-f3c8-49b7-a960-20dff648b78c
Davidson, Sean M.
b8eeed87-5d86-42ca-8844-25bf6887253c
McCormick, James
9f5d47a6-87d4-48c3-a952-4133b710bbb1
Barry, Sean
b65013c6-a911-44ee-a98f-3ff7420cced8
Lawrence, Kevin M.
ff8347b7-930c-4414-beab-65f6d6514b73
Knight, Richard A.
da6172f8-cacc-4330-871a-85dea9e893a4
Hubank, Michael
cd19379f-9a05-4891-9c7c-1f6f24d7a13b
Chen, Phang-Lang
6225ade7-1868-4cd2-a767-d2ca35d6433f
Latchman, David S.
71e9db7c-9075-4b49-afac-6413085378db
Stephanou, Anastasis
e9d502e8-693c-4458-a3c6-5e2844665db3

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).

Record type: Article

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.

This record has no associated files available for download.

More information

Published date: 2005
Keywords: ATM, cell cycle, Chk2, 53BP1, MDC1, STAT-1

Identifiers

Local EPrints ID: 26646
URI: http://eprints.soton.ac.uk/id/eprint/26646
ISSN: 0021-9533
PURE UUID: 747654cf-3836-4d68-89c4-ef44222bc6a2
ORCID for Mark S. Cragg: ORCID iD orcid.org/0000-0003-2077-089X

Catalogue record

Date deposited: 10 Apr 2006
Last modified: 10 Nov 2021 02:53

Export record

Altmetrics

Contributors

Author: Paul A. Townsend
Author: Mark S. Cragg ORCID iD
Author: Sean M. Davidson
Author: James McCormick
Author: Sean Barry
Author: Kevin M. Lawrence
Author: Richard A. Knight
Author: Michael Hubank
Author: Phang-Lang Chen
Author: David S. Latchman
Author: Anastasis Stephanou

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×