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哺乳动物雷帕霉素靶蛋白复合物 1(mTORC1)受低氧的调节:原因与后果。

Regulation of mammalian target of rapamycin complex 1 (mTORC1) by hypoxia: causes and consequences.

机构信息

Center for Childhood Cancer, Nationwide Children's Hospital, Columbus, OH 43205, USA.

出版信息

Target Oncol. 2011 Jun;6(2):95-102. doi: 10.1007/s11523-011-0173-x. Epub 2011 Apr 16.

DOI:10.1007/s11523-011-0173-x
PMID:21499767
Abstract

Integration of cellular and extracellular signals maintains tissue homeostasis under conditions of normal proliferation and stress. A central player in regulating responses to stress is the serine/threonine kinase mammalian target of rapamycin (mTOR). In many cancers, mTOR complex 1 (mTORC1) signaling is enhanced, even under conditions where such signaling should be suppressed. This article reviews some of the details that are emerging on how low oxygen (hypoxia) regulates mTORC1 signaling, and the consequences for dysregulation in pediatric solid tumors.

摘要

细胞内和细胞外信号的整合在正常增殖和应激条件下维持组织稳态。调节应激反应的核心参与者是丝氨酸/苏氨酸激酶哺乳动物雷帕霉素靶蛋白(mTOR)。在许多癌症中,即使在应该抑制这种信号的情况下,mTOR 复合物 1(mTORC1)信号也会增强。本文综述了一些关于低氧(缺氧)如何调节 mTORC1 信号的细节,以及这些细节对儿科实体瘤失调的影响。

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mTORC1 signaling under hypoxic conditions is controlled by ATM-dependent phosphorylation of HIF-1α.在缺氧条件下,mTORC1 信号受 ATM 依赖性磷酸化 HIF-1α的控制。
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