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压力来袭:磷酸肌醇介导细胞应激反应。

Stress-ING out: phosphoinositides mediate the cellular stress response.

作者信息

Bunce Matthew W, Gonzales Michael L, Anderson Richard A

机构信息

Department of Pharmacology, University of Wisconsin, Madison, WI 53706, USA.

出版信息

Sci STKE. 2006 Nov 7;2006(360):pe46. doi: 10.1126/stke.3602006pe46.

Abstract

Phosphoinositides regulate numerous cellular processes required for growth, proliferation, and motility. Whereas phosphoinositide signal transduction pathways within the cytosol have been well characterized, nuclear signaling pathways remain poorly understood. Accumulating experimental data have now started to uncover critical functions for nuclear phosphoinositides. In particular, phosphoinositides modulate the activity of the tumor suppressor protein ING2 in response to extracellular stress. These findings highlight a previously uncharacterized function for phosphoinositides and implicate their metabolism in signaling pathways critical for cell survival.

摘要

磷脂酰肌醇调节生长、增殖和运动所需的众多细胞过程。虽然胞质溶胶中的磷脂酰肌醇信号转导途径已得到充分表征,但核信号转导途径仍知之甚少。越来越多的实验数据现已开始揭示核磷脂酰肌醇的关键功能。特别是,磷脂酰肌醇可响应细胞外应激调节肿瘤抑制蛋白ING2的活性。这些发现突出了磷脂酰肌醇以前未被描述的功能,并表明它们的代谢参与了对细胞存活至关重要的信号通路。

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