GSK3 is required for rapalogs to induce degradation of some oncogenic proteins and to suppress cancer cell growth

Junghui Koo(Winship Cancer Institute), Shi‐Yong Sun(Emory University)

Oncotarget

March 12, 2015

10.18632/oncotarget.3291

Cited by 21

Related Papers

The Proteasome Inhibitor PS-341 (Bortezomib) Up-Regulates DR5 Expression Leading to Induction of Apoptosis and Enhancement of TRAIL-Induced Apoptosis Despite Up-Regulation of c-FLIP and Survivin Expression in Human NSCLC Cells

|Cancer Research|2007|164

Enhancing Mammalian Target of Rapamycin (mTOR)–Targeted Cancer Therapy by Preventing mTOR/Raptor Inhibition-Initiated, mTOR/Rictor-Independent Akt Activation

|Cancer Research|2008|159

Proteasome Inhibitor PS-341 (Bortezomib) Induces Calpain-dependent IκBα Degradation

|Journal of Biological Chemistry|2010|98

Rictor Undergoes Glycogen Synthase Kinase 3 (GSK3)-dependent, FBXW7-mediated Ubiquitination and Proteasomal Degradation

|Journal of Biological Chemistry|2015|98

The E3 ubiquitin ligases β-TrCP and FBXW7 cooperatively mediates GSK3-dependent Mcl-1 degradation induced by the Akt inhibitor API-1, resulting in apoptosis

|Molecular Cancer|2013|73