ASCIZ/ATMIN is dispensable for ATM signaling in response to replication stress
- Journal Title
- DNA Repair
- Publication Type
- Journal Article
- Abstract
- The ATM kinase plays critical roles in the response to DNA double-strand breaks, and can also be activated by prolonged DNA replication blocks. It has recently been proposed that replication stress-dependent ATM activation is mediated by ASCIZ (also known as ATMIN, ZNF822), an essential developmental transcription factor. In contrast, we show here that ATM activation, and phosphorylation of its substrates KAP1, p53 and H2AX in response to the replication blocking agent aphidicolin was unaffected in both immortalized and primary ASCIZ/ATMIN-deficient murine embryonic fibroblasts compared to control cells. Similar results were also obtained in human ASCIZ/ATMIN-deleted lymphoma cells. The results demonstrate that ASCIZ/ATMIN is dispensable for ATM activation, and contradict the previously reported dependence of ATM on ASCIZ/ATMIN.
- Publisher
- Elsevier
- Research Division(s)
- Molecular Genetics Of Cancer
- PubMed ID
- 28648892
- Publisher's Version
- https://doi.org/10.1016/j.dnarep.2017.06.022
- Open Access at Publisher's Site
http://www.sciencedirect.com/science/article/pii/S1568786417301349- NHMRC Grants
- NHMRC/1086291,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2017-07-26 12:48:12
Last Modified: 2017-07-26 03:09:08