AI Article Synopsis
Article Abstract
The final sentence of the Acknowledgements should be as follows: This work was supported by grants from Instituto de Salud Carlos III (BA15/00092), Spanish Ministry of Economy and Competitiveness/EU-ERDF (SAF2016-80626-R, SAF2013-49149-R, BFU2014-51672-REDC), Fundación CajaCanarias (AP2015/008) to RF, and the Australian National Health and Medical Research (NHMRC program grant to SRL and KKK (APP1017028).
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/s41388-019-0753-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Correction: DUB3 and USP7 de-ubiquitinating enzymes control replication inhibitor Geminin: molecular characterization and associations with breast cancer.
Oncogene
June 2019
Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Tecnologías Biomédicas, La Laguna, Spain.
The final sentence of the Acknowledgements should be as follows: This work was supported by grants from Instituto de Salud Carlos III (BA15/00092), Spanish Ministry of Economy and Competitiveness/EU-ERDF (SAF2016-80626-R, SAF2013-49149-R, BFU2014-51672-REDC), Fundación CajaCanarias (AP2015/008) to RF, and the Australian National Health and Medical Research (NHMRC program grant to SRL and KKK (APP1017028).
View Article and Find Full Text PDFDUB3 and USP7 de-ubiquitinating enzymes control replication inhibitor Geminin: molecular characterization and associations with breast cancer.
Oncogene
August 2017
Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Tecnologías Biomédicas, La Laguna, Spain.
Correct control of DNA replication is crucial to maintain genomic stability in dividing cells. Inappropriate re-licensing of replicated origins is associated with chromosomal instability (CIN), a hallmark of cancer progression that at the same time provides potential opportunities for therapeutic intervention. Geminin is a critical inhibitor of the DNA replication licensing factor Cdt1.
View Article and Find Full Text PDFDub3 controls DNA damage signalling by direct deubiquitination of H2AX.
Mol Oncol
July 2014
Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Tecnologías Biomédicas, Ofra s/n La Cuesta, La Laguna 38320, Tenerife, Spain. Electronic address:
A crucial event in the DNA damage response is the phosphorylation and subsequent ubiquitination of H2AX, required for the recruitment of proteins involved in DNA repair. Here we identify a novel regulator of this process, the ubiquitin hydrolase Dub3. Overexpression of wild type, but not catalytic inactive, Dub3 decreases the DNA damage-induced mono-ubiquitination of H2A(X) whereas downregulation of Dub3 has the opposite effect.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!