Abstract
In mammalian cells, the tumor suppressor p53 is activated upon a variety of cellular stresses and ensures an appropriate response ranging from arrest and repair to the induction of senescence and apoptosis. Quantitative measurements in individual living cells showed stimulus-dependent dynamics of p53 accumulation upon stress induction. Due to the complexity of the underlying biochemical interactions, mathematical models were indispensable for understanding the topology of the network regulating p53 dynamics. Recent work provides further insights into the causes of heterogeneous responses in individual cells, the rewiring of the network in response to different inputs and the role of the downstream processes in determining the cellular fate upon stress.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 54-59 |
| Number of pages | 6 |
| Journal | Current Opinion in Systems Biology |
| Volume | 3 |
| DOIs | |
| State | Published - Jun 2017 |
| Externally published | Yes |
Bibliographical note
Funding Information:We thank members of our laboratories for helpful discussion. This work was supported by the Intramural Research Program of the Center for Cancer Research, National Cancer Institute, National Institutes of Health (E.B.) and the German Research Foundation ( SPP 1395 , “InKoMBio” to A.L.).
Funding Information:
We thank members of our laboratories for helpful discussion. This work was supported by the Intramural Research Program of the Center for Cancer Research, National Cancer Institute, National Institutes of Health (E.B.) and the German Research Foundation (SPP 1395, "InKoMBio" to A.L.).
Publisher Copyright:
© 2017 Elsevier Ltd.