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sensing and integration of erk and pi3k signals by myc传感和集成myc的erk和pi3k信号
Sensing and Integration of Erk and PI3K Signals by Myc
1 2,3 2,3 1,2
Tae Lee , Guang Yao , Joseph Nevins , Lingchong You *
1 Department of Biomedical Engineering, Duke University, Durham, North Carolina, United States of America, 2 Institute for Genome Sciences and Policy, Duke University,
Durham, North Carolina, United States of America, 3 Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, United
States of America
Abstract
The transcription factor Myc plays a central role in regulating cell-fate decisions, including proliferation, growth, and
apoptosis. To maintain a normal cell physiology, it is critical that the control of Myc dynamics is precisely orchestrated.
Recent studies suggest that such control of Myc can be achieved at the post-translational level via protein stability
modulation. Myc is regulated by two Ras effector pathways: the extracellular signal-regulated kinase (Erk) and
phosphatidylinositol 3-kinase (PI3K) pathways. To gain quantitative insight into Myc dynamics, we have developed a
mathematical model to analyze post-translational regulation of Myc via sequential phosphorylation by Erk and PI3K. Our
results suggest that Myc integrates Erk and PI3K signals to result in various cellular responses by differential stability control
of Myc protein isoforms. Such signal integration confers a flexible dynamic range for the system output, governed by
stability change. In addition, signal integration may require saturation of the input signals, leading to sensitive signal
integration to the temporal features of the input signals, insensitive response to t
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