Rapid turnover of GATA‐2 via ubiquitin‐proteasome protein degradation pathway

摘要: Transcription factor GATA-2 is expressed in a number of tissues, including hematopoietic stem and progenitor cells, crucial for the proliferation survival cells. To further characterize function GATA-2, we examined cellular turnover mechanism GATA-2. In P815 half-life endogenous was found to be as short 30 min after cycloheximide treatment. This reproducible other neuroblastoma cell lines with moderate variation. We also that ultraviolet (UV)-C irradiation markedly represses protein level by facilitating degradation process. Since treatment cells proteasome inhibitor MG132 or clasto-Lactacystin substantially abrogated effects UV-C increased expression both transfected seems occur through pathway. Structure-function analyses GAL4-DNA binding domain (GBD)-GATA-2 fusion deletion mutants suggested regulatory elements reside three regions, two which overlap transactivation domain. detected poly ubiquitinated forms Taken together, these results demonstrate turned over rapidly ubiquitin-proteasome