| First Author | Cao N | Year | 2016 |
| Journal | BMC Mol Biol | Volume | 17 |
| Issue | 1 | Pages | 12 |
| PubMed ID | 27159997 | Mgi Jnum | J:248449 |
| Mgi Id | MGI:6094469 | Doi | 10.1186/s12867-016-0065-9 |
| Citation | Cao N, et al. (2016) A potential role for protein palmitoylation and zDHHC16 in DNA damage response. BMC Mol Biol 17(1):12 |
| abstractText | BACKGROUND: Cells respond to DNA damage by activating the phosphatidylinositol-3 kinase-related kinases, p53 and other pathways to promote cell cycle arrest, apoptosis, and/or DNA repair. Here we report that protein palmitoylation, a modification carried out by protein acyltransferases with zinc-finger and Asp-His-His-Cys domains (zDHHC), is required for proper DNA damage responses. RESULTS: Inhibition of protein palmitoylation compromised DNA damage-induced activation of Atm, induction and activation of p53, cell cycle arrest at G2/M phase, and DNA damage foci assembly/disassembly in primary mouse embryonic fibroblasts. Furthermore, knockout of zDHHC16, a palmitoyltransferase gene identified as an interacting protein for c-Abl, a non-receptor tyrosine kinase involved in DNA damage response, reproduced most of the defects in DNA damage responses produced by the inhibition of protein palmitoylation. CONCLUSIONS: Our results revealed critical roles for protein palmitoylation and palmitoyltransferase zDHHC16 in early stages of DNA damage responses and in the regulation of Atm activation. |
