Unraveling the regulation of mTORC2 using logical modeling

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• 作者：Kirsten Thobe ; Christine Sers ; Heike Siebert
• 关键词：Logical modeling ; mTORC2 regulation ; Cancer signaling
• 刊名：Cell Communication and Signaling
• 出版年：2017
• 出版时间：December 2017
• 年：2017
• 卷：15
• 期：1
• 全文大小：1215KB
• 刊物主题：Cell Biology; Protein-Ligand Interactions; Receptors; Cytokines and Growth Factors;
• 出版者：BioMed Central
• ISSN：1478-811X
• 卷排序：15

文摘

BackgroundThe mammalian target of rapamycin (mTOR) is a regulator of cell proliferation, cell growth and apoptosis working through two distinct complexes: mTORC1 and mTORC2. Although much is known about the activation and inactivation of mTORC1, the processes controlling mTORC2 remain poorly characterized. Experimental and modeling studies have attempted to explain the regulation of mTORC2 but have yielded several conflicting hypotheses. More specifically, the Phosphoinositide 3-kinase (PI3K) pathway was shown to be involved in this process, but the identity of the kinase interacting with and regulating mTORC2 remains to be determined (Cybulski and Hall, Trends Biochem Sci 34:620-7, 2009).