Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation

Search Page

Filters

My NCBI Filters

Results by year

Table representation of search results timeline featuring number of search results per year.

Year Number of Results
2013 1
2014 1
2016 1
2017 1
2018 2
2020 2
2021 4
2024 0

Text availability

Article attribute

Article type

Publication date

Search Results

12 results

Results by year

Filters applied: . Clear all
Page 1
Reactive oxygen species and DNA damage response in cancer.
Renaudin X. Renaudin X. Int Rev Cell Mol Biol. 2021;364:139-161. doi: 10.1016/bs.ircmb.2021.04.001. Epub 2021 May 3. Int Rev Cell Mol Biol. 2021. PMID: 34507782 Review.
Compared with normal cells, cancer cells often have an increase in reactive oxygen species (ROS) level. ...Increase of ROS can be due to increase of production or decrease of detoxification, both situations being well described in various cancers. Oxidative stress i …
Compared with normal cells, cancer cells often have an increase in reactive oxygen species (ROS) level. ...Increase of ROS can be due …
The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.
Renaudin X, Rosselli F. Renaudin X, et al. Genes (Basel). 2020 May 25;11(5):585. doi: 10.3390/genes11050585. Genes (Basel). 2020. PMID: 32466131 Free PMC article. Review.
ICL accumulation results in growth arrest and cell death-particularly in cell populations undergoing high replicative activity, such as cancer and leukemic cells. For this reason, agents able to induce DNA ICLs are widely used as chemotherapeutic drugs. ...Therefore, every …
ICL accumulation results in growth arrest and cell death-particularly in cell populations undergoing high replicative activity, such as c …
The ubiquitin family meets the Fanconi anemia proteins.
Renaudin X, Koch Lerner L, Menck CF, Rosselli F. Renaudin X, et al. Mutat Res Rev Mutat Res. 2016 Jul-Sep;769:36-46. doi: 10.1016/j.mrrev.2016.06.004. Epub 2016 Jun 23. Mutat Res Rev Mutat Res. 2016. PMID: 27543315 Review.
Fanconi anaemia (FA) is a hereditary disorder characterized by bone marrow failure, developmental defects, predisposition to cancer and chromosomal abnormalities. FA is caused by biallelic mutations that inactivate genes encoding proteins involved in replication stress-ass …
Fanconi anaemia (FA) is a hereditary disorder characterized by bone marrow failure, developmental defects, predisposition to cancer a …
A kinase-independent function for AURORA-A in replisome assembly during DNA replication initiation.
Guarino Almeida E, Renaudin X, Venkitaraman AR. Guarino Almeida E, et al. Among authors: renaudin x. Nucleic Acids Res. 2020 Aug 20;48(14):7844-7855. doi: 10.1093/nar/gkaa570. Nucleic Acids Res. 2020. PMID: 32652013 Free PMC article.
The catalytic activity of human AURORA-A kinase (AURKA) regulates mitotic progression, and its frequent overexpression in major forms of epithelial cancer is associated with aneuploidy and carcinogenesis. Here, we report an unexpected, kinase-independent function for AURKA …
The catalytic activity of human AURORA-A kinase (AURKA) regulates mitotic progression, and its frequent overexpression in major forms of epi …
A Class of Environmental and Endogenous Toxins Induces BRCA2 Haploinsufficiency and Genome Instability.
Tan SLW, Chadha S, Liu Y, Gabasova E, Perera D, Ahmed K, Constantinou S, Renaudin X, Lee M, Aebersold R, Venkitaraman AR. Tan SLW, et al. Among authors: renaudin x. Cell. 2017 Jun 1;169(6):1105-1118.e15. doi: 10.1016/j.cell.2017.05.010. Cell. 2017. PMID: 28575672 Free PMC article.
Mutations truncating a single copy of the tumor suppressor, BRCA2, cause cancer susceptibility. In cells bearing such heterozygous mutations, we find that a cellular metabolite and ubiquitous environmental toxin, formaldehyde, stalls and destabilizes DNA replication forks, …
Mutations truncating a single copy of the tumor suppressor, BRCA2, cause cancer susceptibility. In cells bearing such heterozygous mu …
BRCA2 deficiency reveals that oxidative stress impairs RNaseH1 function to cripple mitochondrial DNA maintenance.
Renaudin X, Lee M, Shehata M, Surmann EM, Venkitaraman AR. Renaudin X, et al. Cell Rep. 2021 Aug 3;36(5):109478. doi: 10.1016/j.celrep.2021.109478. Cell Rep. 2021. PMID: 34348152 Free PMC article.
Oxidative stress is a ubiquitous cellular challenge implicated in aging, neurodegeneration, and cancer. By studying pathogenic mutations in the tumor suppressor BRCA2, we identify a general mechanism by which oxidative stress restricts mitochondrial (mt)DNA replication. .. …
Oxidative stress is a ubiquitous cellular challenge implicated in aging, neurodegeneration, and cancer. By studying pathogenic mutati …
A mitochondrial response to oxidative stress mediated by unscheduled RNA-DNA hybrids (R-loops).
Renaudin X, Venkitaraman AR. Renaudin X, et al. Mol Cell Oncol. 2021 Dec 14;8(6):2007028. doi: 10.1080/23723556.2021.2007028. eCollection 2021. Mol Cell Oncol. 2021. PMID: 35419470 Free PMC article.
How oxidative stress promotes aging-related human diseases like cancer and neurodegeneration remains unclear. Here, we discuss the origins and implications of an oxidative-stress response recently reported to destabilize the mitochondrial (mt) genome via unscheduled RNA/DN …
How oxidative stress promotes aging-related human diseases like cancer and neurodegeneration remains unclear. Here, we discuss the or …
Germline BAP1 mutations predispose to renal cell carcinomas.
Popova T, Hebert L, Jacquemin V, Gad S, Caux-Moncoutier V, Dubois-d'Enghien C, Richaudeau B, Renaudin X, Sellers J, Nicolas A, Sastre-Garau X, Desjardins L, Gyapay G, Raynal V, Sinilnikova OM, Andrieu N, Manié E, de Pauw A, Gesta P, Bonadona V, Maugard CM, Penet C, Avril MF, Barillot E, Cabaret O, Delattre O, Richard S, Caron O, Benfodda M, Hu HH, Soufir N, Bressac-de Paillerets B, Stoppa-Lyonnet D, Stern MH. Popova T, et al. Among authors: renaudin x. Am J Hum Genet. 2013 Jun 6;92(6):974-80. doi: 10.1016/j.ajhg.2013.04.012. Epub 2013 May 16. Am J Hum Genet. 2013. PMID: 23684012 Free PMC article.
We then screened for germline BAP1 deleterious mutations in familial aggregations of cancers within the spectrum of the recently described BAP1-associated tumor predisposition syndrome, including uveal melanoma, malignant pleural mesothelioma, and cutaneous melanoma. ...
We then screened for germline BAP1 deleterious mutations in familial aggregations of cancers within the spectrum of the recently desc …
BRCA2 controls DNA:RNA hybrid level at DSBs by mediating RNase H2 recruitment.
D'Alessandro G, Whelan DR, Howard SM, Vitelli V, Renaudin X, Adamowicz M, Iannelli F, Jones-Weinert CW, Lee M, Matti V, Lee WTC, Morten MJ, Venkitaraman AR, Cejka P, Rothenberg E, d'Adda di Fagagna F. D'Alessandro G, et al. Among authors: renaudin x. Nat Commun. 2018 Dec 18;9(1):5376. doi: 10.1038/s41467-018-07799-2. Nat Commun. 2018. PMID: 30560944 Free PMC article.
BRCA2 Regulates Transcription Elongation by RNA Polymerase II to Prevent R-Loop Accumulation.
Shivji MKK, Renaudin X, Williams ÇH, Venkitaraman AR. Shivji MKK, et al. Among authors: renaudin x. Cell Rep. 2018 Jan 23;22(4):1031-1039. doi: 10.1016/j.celrep.2017.12.086. Epub 2018 Jan 28. Cell Rep. 2018. PMID: 29386125 Free PMC article.
We show that the human tumor suppressor BRCA2 interacts with RNAPII to regulate PPP release, thereby preventing unscheduled RNA-DNA hybrids (R-loops) implicated in genomic instability and carcinogenesis. BRCA2 inactivation by depletion or cancer-causing mutations instigate …
We show that the human tumor suppressor BRCA2 interacts with RNAPII to regulate PPP release, thereby preventing unscheduled RNA-DNA hybrids …
12 results