Ulsamer, ArnauMartínez Limón, AdriánBader, SRodríguez Acebes, SaraFreire, RaimundoMéndez, JuanNadal Clanchet, Eulàlia dePosas, Francesc2025-04-252025-04-252022-09-202211-1247https://hdl.handle.net/2445/220608Stress-activated protein kinases (SAPKs) enhance survival in response to environmental changes. In yeast, the Hog1 SAPK and Mrc1, a protein required for DNA replication, define a safeguard mechanism that allows eukaryotic cells to prevent genomic instability upon stress during S-phase. Here we show that, in mammals, the p38 SAPK and Claspin-the functional homolog of Mrc1-protect cells from DNA damage upon osmostress during S-phase. We demonstrate that p38 phosphorylates Claspin and either the mutation of the p38-phosphorylation sites in Claspin or p38 inhibition suppresses the protective role of Claspin on DNA damage. In addition, wild-type Claspin but not the p38-unphosphorylatable mutant has a protective effect on cell survival in response to cisplatin treatment. These findings reveal a role of Claspin in response to chemotherapeutic drugs. Thus, this pathway protects S-phase integrity from different insults and it is conserved from yeast to mammals.17 p.application/pdfengcc-by-nc-nd (c) Ulsamer, Arnau et al., 2022http://creativecommons.org/licenses/by-nc-nd/3.0/es/ADNEstrès (Fisiologia)Cicle cel·lularCisplatíDNAStress (Physiology)Cell cycleCisplatininfo:eu-repo/semantics/article2025-04-23info:eu-repo/semantics/openAccess656754036130506