| First Author | Hernandez VJ | Year | 2013 |
| Journal | Elife | Volume | 2 |
| Pages | e00905 | PubMed ID | 24069528 |
| Mgi Jnum | J:202374 | Mgi Id | MGI:5518817 |
| Doi | 10.7554/eLife.00905 | Citation | Hernandez VJ, et al. (2013) Cavin-3 dictates the balance between ERK and Akt signaling. Elife 2:e00905 |
| abstractText | Cavin-3 is a tumor suppressor protein of unknown function. Using both in vivo and in vitro approaches, we show that cavin-3 dictates the balance between ERK and Akt signaling. Loss of cavin-3 increases Akt signaling at the expense of ERK, while gain of cavin-3 increases ERK signaling at the expense Akt. Cavin-3 facilitates signal transduction to ERK by anchoring caveolae to the membrane skeleton of the plasma membrane via myosin-1c. Caveolae are lipid raft specializations that contain an ERK activation module and loss of the cavin-3 linkage reduces the abundance of caveolae, thereby separating this ERK activation module from signaling receptors. Loss of cavin-3 promotes Akt signaling through suppression of EGR1 and PTEN. The in vitro consequences of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cell proliferation, and resistance to apoptosis. The in vivo consequences of cavin-3 knockout are increased lactate production and cachexia. DOI:http://dx.doi.org/10.7554/eLife.00905.001. |
