Regulation of mammalian target of rapamycin complex 1 (mTORC1) by hypoxia: causes and consequences
Identifieur interne : 001515 ( Main/Exploration ); précédent : 001514; suivant : 001516Regulation of mammalian target of rapamycin complex 1 (mTORC1) by hypoxia: causes and consequences
Auteurs : Hakan Cam [États-Unis] ; Peter J. Houghton [États-Unis]Source :
- Targeted Oncology [ 1776-2596 ] ; 2011-06-01.
English descriptors
- KwdEn :
Abstract
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.
Url:
DOI: 10.1007/s11523-011-0173-x
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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