par Delatte, Benjamin
;Jeschke, Jana
;Defrance, Matthieu
;Bachman, Martin;Creppe, Catherine
;Calonne, Emilie
;Bizet, Martin
;Deplus, Rachel
;Marroquí, Laura
;Libin, Myriam
;Ravichandran, Mirunalini;Mascart, Françoise
;Eizirik, Decio L.
;Murrell, Adele;Jurkowski, Tomasz Piotr;Fuks, François 
Référence Scientific reports, 5, page (12714)
Publication Publié, 2015-08
;Jeschke, Jana
;Defrance, Matthieu
;Bachman, Martin;Creppe, Catherine
;Calonne, Emilie
;Bizet, Martin
;Deplus, Rachel
;Marroquí, Laura
;Libin, Myriam
;Ravichandran, Mirunalini;Mascart, Françoise
;Eizirik, Decio L.
;Murrell, Adele;Jurkowski, Tomasz Piotr;Fuks, François 
Référence Scientific reports, 5, page (12714)
Publication Publié, 2015-08
Article révisé par les pairs
| Résumé : | The TET enzymes convert methylcytosine to the newly discovered base hydroxymethylcytosine. While recent reports suggest that TETs may play a role in response to oxidative stress, this role remains uncertain, and results lack in vivo models. Here we show a global decrease of hydroxymethylcytosine in cells treated with buthionine sulfoximine, and in mice depleted for the major antioxidant enzymes GPx1 and 2. Furthermore, genome-wide profiling revealed differentially hydroxymethylated regions in coding genes, and intriguingly in microRNA genes, both involved in response to oxidative stress. These results thus suggest a profound effect of in vivo oxidative stress on the global hydroxymethylome. |



