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- W2054336789 abstract "The directed migration of cells in response to chemical cues, known as chemotaxis, plays a critical role in normal physiology and disease pathogenesis. Knowledge of the molecular mechanism of chemotaxis is critical to our understanding of the process of metastasis and for developing new therapies to prevent it.During chemotaxis ‘front’ proteins are recruited to extending pseudopods, which themselves are concentrated at the cell's anterior. Conversely, ‘back’ proteins dissociate from nascent pseudopods.The Ras/TorC2 pathway has recently been shown to be important for chemotaxis in Dictyostelium. A similar conserved mTORC2 pathway has since been shown to play a role in neutrophil chemotaxis. The discovery of the importance of this pathway in chemotaxis challenges the conventional linear, PIP3-centric view of chemotaxis, in favor of a model involving a complex network of parallel pathways connected via feedback mechanisms.In an attempt to decipher the mechanism of chemotaxis we generated pairwise mutations activating front protein RasC, and inactivating back-protein PTEN. Here we report that this combination of RasC and PTEN perturbations trapped cells in a globally activated or ‘front-state’. Front-state “clamped” cells in Dictyostelium were extremely spread and flattened. Most surprising was the susceptibility of these altered cells to death by cytoplasmic fragmentation.Front state clamped cells displayed global elevations of front protein signaling at the cortex. Levels of actin-binding probe GFP LimE at the cortex of front-state cells were elevated, as they were at the peak of the chemotactic response at the tips of pseudopods in control cells.The promise of this research is rooted in our discovery of a potentially specific vulnerability of eukaryotic cells with a combination of mutations to PTEN and Ras; two genes commonly mutated in human cancers." @default.
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- W2054336789 date "2015-01-01" @default.
- W2054336789 modified "2023-09-28" @default.
- W2054336789 title "Persistent Activation of Signal Transduction Networks Induces a Novel Mechanism of Cell Death" @default.
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