ArticleExperimental cell research2007
Akt shows variable sensitivity to an Hsp90 inhibitor depending on cell context.
Article in Experimental cell research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Evaluation of Hsp90 and mTOR inhibitors as potential drugs for the treatment of TSC1/TSC2 deficient cancer.PloS one · 2021Article
- SUV39H1 is a New Client Protein of Hsp90 Degradated by Chaetocin as a Novel C-Terminal Inhibitor of Hsp90.Biomolecules & therapeutics · 2021Article
- Control of Akt activity and substrate phosphorylation in cells.IUBMB life · 2020Review
- Getting the Akt Together: Guiding Intracellular Akt Activity by PI3K.Biomolecules · 2019Review
- Mutational Analysis of Glycogen Synthase Kinase 3β Protein Kinase Together with Kinome-Wide Binding and Stability Studies Suggests Context-Dependent Recognition of Kinases by the Chaperone Heat Shock Protein 90.Molecular and cellular biology · 2016Article
- A network of ubiquitin ligases is important for the dynamics of misfolded protein aggregates in yeast.The Journal of biological chemistry · 2012Article
- Article
- Fibroblast growth factor receptor 3 (FGFR3) is a strong heat shock protein 90 (Hsp90) client: implications for therapeutic manipulation.The Journal of biological chemistry · 2011Article
- Hsp110 chaperones control client fate determination in the hsp70-Hsp90 chaperone system.Molecular biology of the cell · 2010Article
- Physiological regulation of Akt activity and stability.American journal of translational research · 2010Article
- Article
- BI-69A11-mediated inhibition of AKT leads to effective regression of xenograft melanoma.Pigment cell & melanoma research · 2009Article
- Targeting the oncogene and kinome chaperone CDC37.Nature reviews. Cancer · 2008Review
- Ydj1 protects nascent protein kinases from degradation and controls the rate of their maturation.Molecular and cellular biology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hsp90 inhibitors are currently in clinical trials for cancer therapy based on their ability to promote proteasomal degradation of oncogenic protein kinases and nuclear receptors. Results from recent studies suggest that cancer cells are more sensitive to these inhibitors than cells from healthy tissues. We analyzed an immortalized cell line Ba/F3 for sensitivity to the Hsp90 inhibitor geldanamycin in the absence and presence of the oncogenic tyrosine fusion kinase NPM-ALK expressed from a retroviral vector. Our results showed that NPM-ALK expression makes Akt and Cdk4 more resistant to degradation in the presence of geldanamycin, and there was a slightly reduced amount of apoptosis. The mechanism underlying the effect of NPM-ALK on Akt stability was probed by comparison of the turnover of the kinase after translation inhibition and geldanamycin treatment. We observed that Akt was degraded more rapidly in the presence of GA than upon translation inhibition without NPM-ALK expression. This suggests that NPM-ALK protects the mature kinase. Furthermore, Akt failed to bind to the Cdc37 chaperone in cells expressing NPM-ALK, which also correlates with increased Akt stability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.