English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
  A Comprehensive Analysis of the Dynamic Response to Aphidicolin-Mediated Replication Stress Uncovers Targets for ATM and ATMIN

Mazouzi, A., Stukalov, A., Müller, A. C., Chen, D., Wiedner, M., Prochazkova, J., et al. (2016). A Comprehensive Analysis of the Dynamic Response to Aphidicolin-Mediated Replication Stress Uncovers Targets for ATM and ATMIN. CELL REPORTS, 15(4), 893-908. doi:10.1016/j.celrep.2016.03.077.

Item is

Basic

show hide
Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-E356-1 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-E357-0
Genre: Journal Article

Files

show Files
hide Files
:
1-s2.0-S2211124716303667-main.pdf (Any fulltext), 7MB
Name:
1-s2.0-S2211124716303667-main.pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
open access article
License:
-

Locators

show

Creators

show
hide
 Creators:
Mazouzi, Abdelghani1, Author
Stukalov, Alexey2, Author              
Müller, Andre C.1, Author
Chen, Doris1, Author
Wiedner, Marc1, Author
Prochazkova, Jana1, Author
Chiang, Shih-Chieh1, Author
Schuster, Michael1, Author
Breitwieser, Florian P.1, Author
Pichlmair, Andreas2, Author              
El-Khamisy, Sherif F.1, Author
Bock, Christoph1, Author
Kralovics, Robert1, Author
Colinge, Jacques1, Author
Bennett, Keiryn L.1, Author
Loizou, Joanna I.1, Author
Affiliations:
1external, ou_persistent22              
2Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565166              

Content

show
hide
Free keywords: STRAND BREAK REPAIR; DNA-DAMAGE; HISTONE H2AX; CANCER DEVELOPMENT; FRAGILE SITES; ACTIVATION; RECRUITMENT; 53BP1; P53; PHOSPHORYLATION
 Abstract: The cellular response to replication stress requires the DNA-damage-responsive kinase ATM and its cofactor ATMIN; however, the roles of this signaling pathway following replication stress are unclear. To identify the functions of ATM and ATMIN in response to replication stress, we utilized both transcriptomics and quantitative mass-spectrometry-based phosphoproteomics. We found that replication stress induced by aphidicolin triggered widespread changes in both gene expression and protein phosphorylation patterns. These changes gave rise to distinct early and late replication stress responses. Furthermore, our analysis revealed previously unknown targets of ATM and ATMIN downstream of replication stress. We demonstrate ATMIN-dependent phosphorylation of H2AX and of CRMP2, a protein previously implicated in Alzheimer's disease but not in the DNA damage response. Overall, our dataset provides a comprehensive resource for discovering the cellular responses to replication stress and, potentially, associated pathologies.

Details

show
hide
Language(s): eng - English
 Dates: 2016
 Publication Status: Published in print
 Pages: 16
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: CELL REPORTS
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA : CELL PRESS
Pages: - Volume / Issue: 15 (4) Sequence Number: - Start / End Page: 893 - 908 Identifier: ISSN: 2211-1247