• Publications
  • Influence
Akt Forms an Intracellular Complex with Heat Shock Protein 90 (Hsp90) and Cdc37 and Is Destabilized by Inhibitors of Hsp90 Function*
TLDR
Transduction of growth factor signaling via the Akt and Raf pathways requires functional Hsp90 and can be coordinately blocked by its inhibition, which results in a shortening of the half-life of Akt from 36 to 12 h and an 80% reduction in its expression.
Genomic and functional analysis of leukemic transformation of myeloproliferative neoplasms
TLDR
In vitro studies revealed that post-MPN AML cells were sensitive to decitabine, the JAK1/2 inhibitor ruxolitinib, or the heat shock protein 90 inhibitor 8-(6-iodobenzo-5-ylthio)-9-(3-(isopropylamino)propyl)-9H-purine-6-amine (PU-H71).
Roles of heat-shock protein 90 in maintaining and facilitating the neurodegenerative phenotype in tauopathies
TLDR
P35, a neuronal protein that activates cyclin-dependent protein kinase 5 through complex formation leading to aberrant Tau phosphorylation, and that of mutant but not WT Tau protein is maintained in tauopathies by Hsp90, leading to a reduction of the pathogenic activity of these proteins and results in elimination of aggregated Tau.
Hsp90 inhibitor PU-H71, a multimodal inhibitor of malignancy, induces complete responses in triple-negative breast cancer models
TLDR
The results identify Hsp90 as a critical and multimodal target in this most difficult to treat breast cancer subtype and support the use of the Hsp 90 inhibitor PU-H71 for clinical trials involving patients with TNBC.
BCL6 repression of EP300 in human diffuse large B cell lymphoma cells provides a basis for rational combinatorial therapy.
TLDR
RI-BPI induces a particular gene expression signature in human DLBCL cell lines that included genes associated with the actions of histone deacetylase (HDAC) and Hsp90 inhibitors, and p300-inactivating mutations occur naturally in humanDLBCL patients and may confer resistance to BCL6 inhibitors.
BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90.
TLDR
Clinical data support clinical investigations of 17-AAG in imatinib mesylate-resistant Ph(+) leukemias, with a trend indicating more potent activity against mutant BCR-ABL proteins.
Selective compounds define Hsp90 as a major inhibitor of apoptosis in small-cell lung cancer.
TLDR
It is discovered that small-cell lung carcinoma is a distinctive cellular system in which apoptosis is mainly regulated by Hsp90, and this results provide important evidence for a transformation-specific interplay between chaperones in regulating apoptosis in malignant cells.
...
...