| Literature DB >> 15749021 |
Zhi-Xiang Xu1, Wen-Xin Zou, Pei Lin, Kun-Sang Chang.
Abstract
The promyelocytic leukemia gene (PML), which is disrupted by the chromosomal translocation t(15;17) in acute promyelocytic leukemia (APL), encodes a multifunctional protein involved in several important cellular functions. Herein, we demonstrate that PML is localized to centrosomes and that PML deficiency leads to centrosome amplification. By using PML isoform-specific antibodies, we found PML3-specific association with the centrosome and the pole of the mitotic spindle. PML3 deficiency leads to dysregulation of the centrosome duplication checkpoint. Furthermore, PML3 physically interacts with Aurora A and regulates its kinase activity. Specific knockdown of PML3 activates Cdk2/cyclin kinase activity. The results of this study implicate a direct role for PML3 in the control of centrosome duplication through suppression of Aurora A activation to prevent centrosome reduplication.Entities:
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Year: 2005 PMID： 15749021 DOI： 10.1016/j.molcel.2005.02.014
Source DB: PubMed Journal: Mol Cell ISSN： 1097-2765 Impact factor: 17.970