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首页> 外文期刊>Molecular and Cellular Biology >Phosphoinositide 3-Kinase Beta Protects Nuclear Envelope Integrity by Controlling RCC1 Localization and Ran Activity
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Phosphoinositide 3-Kinase Beta Protects Nuclear Envelope Integrity by Controlling RCC1 Localization and Ran Activity

机译：Phosphoinositide 3-Kinase Beta通过控制RCC1定位和Ran活性保护核被膜的完整性。

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摘要

The nuclear envelope (NE) forms a barrier between the nucleus and the cytosol that preserves genomic integrity. The nuclear lamina and nuclear pore complexes (NPCs) are NE components that regulate nuclear events through interaction with other proteins and DNA. Defects in the nuclear lamina are associated with the development of laminopathies. As cells depleted of phosphoinositide 3-kinase beta (PI3Kβ) showed an aberrant nuclear morphology, we studied the contribution of PI3Kβ to maintenance of NE integrity. pik3cb depletion reduced the nuclear membrane tension, triggered formation of areas of lipid bilayer/lamina discontinuity, and impaired NPC assembly. We show that one mechanism for PI3Kβ regulation of NE/NPC integrity is its association with RCC1 (regulator of chromosome condensation 1), the activator of nuclear Ran GTPase. PI3Kβ controls RCC1 binding to chromatin and, in turn, Ran activation. These findings suggest that PI3Kβ regulates the nuclear envelope through upstream regulation of RCC1 and Ran.
机译：核被膜（NE）在核与胞质溶胶之间形成屏障，可保持基因组完整性。核层和核孔复合物（NPC）是通过与其他蛋白质和DNA相互作用调节核事件的NE成分。核椎板的缺陷与椎间盘病变的发展有关。由于耗尽磷酸肌醇3-激酶β（PI3Kβ）的细胞显示出异常的核形态，我们研究了PI3Kβ对维持NE完整性的贡献。 pik3cb 消耗减少了核膜张力，触发了脂质双层/椎板间断区域的形成，并损害了NPC组装。我们表明，PI3Kβ调控NE / NPC完整性的一种机制是其与RCC1（染色体缩合1的调节剂）的结合，RCC1是核Ran GTPase的激活剂。 PI3Kβ控制RCC1与染色质的结合，进而控制Ran激活。这些发现表明PI3Kβ通过RCC1和Ran的上游调节来调节核被膜。

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