BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma
作者： Wondossen Sime , Qiankun Niu , Yasmin Abassi , Katarzyna Chmielarska Masoumi , Reihaneh Zarrizi
DOI: 10.1038/S41419-018-0500-6
关键词:
摘要: BRCA1-associated protein 1 (BAP1) is a nuclear deubiquitinating enzyme that associated with multiprotein complexes regulate key cellular pathways, including cell cycle, differentiation, death, and the DNA damage response. In this study, we found reduced expression of BAP1 pro6motes survival neuroblastoma cells, restoring levels in these cells facilitated delay S G2/M phase as well apoptosis. The mechanism induces death mediated via an interaction 14-3-3 protein. association between releases apoptotic inducer Bax from promotes through intrinsic apoptosis pathway. Xenograft studies confirmed reduces tumor growth progression vivo by lowering pro-survival factors such Bcl-2, which turn diminish potential cells. Patient data analyses finding high-BAP1 mRNA correlates better clinical outcome. summary, our study uncovers new for regulation
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