E-GEOD-50982 - Cavin-3 Dictates the Balance Between ERK and Akt Signaling

Released on 24 September 2013, last updated on 3 June 2014
Homo sapiens
Samples (45)
Array (1)
Protocols (7)
Cavin-3 is a tumor suppressor protein of unknown function. Using a combination of in vivo knockout and in vitro gain/loss of function 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, a lipid-raft specialization that contains an ERK activation module, to the membrane skeleton of the plasma membrane. Loss of cavin-3 reduces the number 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 loss are increased lactate production and cachexia. 9 total samples, consisting of 3 cavin-3 siRNA groups (0 days, 3 days and 8 days) one set was untreated, one set was serum starved, one set was serum starved and then treated with EGF for 1 hr.
Experiment type
transcription profiling by array 
Investigation descriptionE-GEOD-50982.idf.txt
Sample and data relationshipE-GEOD-50982.sdrf.txt
Processed data (1)E-GEOD-50982.processed.1.zip
Additional data (1)E-GEOD-50982.additional.1.zip
Array designA-GEOD-10558.adf.txt