TY  - JOUR
AB  - B-Myb, a highly conserved member of the Myb transcription factor family, is expressed ubiquitously in proliferating cells and controls the cell cycle dependent transcription of G2/M-phase genes. Deregulation of B-Myb has been implicated in oncogenesis and loss of genomic stability. We have identified B-Myb as a novel interaction partner of the Mre11-Rad50-Nbs1 (MRN) complex, a key player in the repair of DNA double strand breaks. We show that B-Myb directly interacts with the Nbs1 subunit of the MRN complex and is recruited transiently to DNA-damage sites. In response to DNA-damage B-Myb is phosphorylated by protein kinase GSK3β and released from the MRN complex. A B-Myb mutant that cannot be phosphorylated by GSK3β disturbs the regulation of pro-mitotic B-Myb target genes and leads to inappropriate mitotic entry in response to DNA-damage. Overall, our work suggests a novel function of B-Myb in the cellular DNA-damage signalling.
AU  - Henrich, Sarah
AU  - Henrich, Sarah Marie
AU  - Usadel, Clemens
AU  - Werwein, Eugen
AU  - Burdová, Kamila
AU  - Janščák, Pavel
AU  - Ferrari, Stefano
AU  - Hess, Daniel
AU  - Klempnauer, Karl-Heinz
DA  - 2017-01-27
DO  - 10.1038/srep41663
LA  - eng
N1  - Scientific Reports 7 (2017), 41663, 1-14
N1  - Finanziert durch den Open-Access-Publikationsfonds 2015/2016 der Westfälischen Wilhelms-Universität Münster (WWU Münster).
PY  - 2017-01-27
SN  - 2045-2322
TI  - Interplay with the Mre11-Rad50-Nbs1 complex and phosphorylation by GSK3β implicate human B-Myb in DNA-damage signaling
UR  - https://nbn-resolving.org/urn:nbn:de:hbz:6-11239615095
Y2  - 2024-11-22T09:06:55
ER  -