Turnover of the mTOR inhibitor, DEPTOR, and downstream AKT phosphorylation in multiple myeloma cells, is dependent on ERK1-mediated phosphorylation
Author:
Funder
NIH
Department of Veterans Affairs
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry
Reference20 articles.
1. DEPTOR is an mTOR inhibitor frequently overexpressed in multiple myeloma cells and required for their survival;Peterson;Cell,2009
2. Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells;Obeng;Blood,2006
3. mTOR generates an auto-amplification loop by triggering the betaTrCP- and CK1alpha-dependent degradation of DEPTOR;Duan;Mol. Cell,2011
4. mTOR drives its own activation via SCFβTrCP-dependent degradation of the mTOR inhibitor DEPTOR;Gao;Mol. Cell,2011
5. DEPTOR, an mTOR inhibitor, is a physiological substrate of SCFβTrCP E3 ubiquitin ligase and regulates survival and autophagy;Zhao;Mol. Cell,2011
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2. Targeting mTOR signaling pathways in multiple myeloma: biology and implication for therapy;Cell Communication and Signaling;2024-06-11
3. Addressing the Reciprocal Crosstalk between the AR and the PI3K/AKT/mTOR Signaling Pathways for Prostate Cancer Treatment;International Journal of Molecular Sciences;2023-01-24
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