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首页> 外文期刊>Nucleus >The tumor suppressor SHIP1 colocalizes in nucleolar cavities with p53 and components of PML nuclear bodies
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The tumor suppressor SHIP1 colocalizes in nucleolar cavities with p53 and components of PML nuclear bodies

机译：抑癌剂SHIP1与p53和PML核小体成分共定位在核仁腔中

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摘要

The inositol 5-phosphatase SHIP1 is a negative regulator of signaling processes in haematopoietic cells. By converting PI(3,4,5)P-3 to PtdIns(3,4)P-2 at the plasma membrane, SHIP1 modifies PI3-kinase mediated signaling. We have recently demonstrated that SHIP1 is a nucleo-cytoplasmic shuttling protein and SHIP1 nuclear puncta partially colocalize with FLASH, a component of nuclear bodies. In this study, we demonstrate that endogenous SHIP1 localizes to intranucleolar regions of both normal and leukemic haematopoietic cells. In addition, we report that ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53 and components of PML nuclear bodies (e. g. SP100, SUMO-1 and CK2). Moreover, SHIP1 also colocalizes in nucleolar cavities with components of the ubiquitin-proteasome pathway. By using confocal microscopy data, we generated 3D-models revealing the enormous extent of the SHIP1 aggresomes in the nucleolus. Furthermore, treatment of cells with the proteasome inhibitor MG132 causes an enlargement of nucleolar SHIP1 containing structures. Unexpectedly, this accumulation can be partially prevented by treatment with the inhibitor of nuclear protein export Leptomycin B. In recent years, several proteins aggregating in nucleolar cavities were shown to be key factors of neurodegenerative diseases and cancerogenesis. Our findings support current relevance of nuclear localized SHIP1.
机译：肌醇5-磷酸酶SHIP1是造血细胞中信号传导过程的负调节剂。通过在质膜上将PI（3,4,5）P-3转换为PtdIns（3,4）P-2，SHIP1修饰了PI3激酶介导的信号传导。我们最近证明，SHIP1是一种核质穿梭蛋白，SHIP1核小点与FLASH（一种核小体的组成部分）共定位。在这项研究中，我们证明内源性SHIP1定位于正常和白血病造血细胞的核内区域。另外，我们报道异位表达的SHIP1在核仁腔中积累并与肿瘤抑制蛋白p53和PML核体的组分（例如SP100，SUMO-1和CK2）共定位。此外，SHIP1还与泛素-蛋白酶体途径的成分共定位在核仁腔中。通过使用共聚焦显微镜数据，我们生成了3D模型，揭示了核仁中SHIP1聚集体的巨大范围。此外，用蛋白酶体抑制剂MG132处理细胞导致含有核仁SHIP1的结构增大。出乎意料的是，可以通过用核蛋白输出的瘦霉素B抑制剂治疗来部分防止这种积累。近年来，核仁腔中聚集的几种蛋白质被证明是神经退行性疾病和癌症发生的关键因素。我们的研究结果支持核本地SHIP1的当前相关性。

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