V600E B-Raf requires the Hsp90 chaperone for stability and is degraded in response to Hsp90 inhibitors
about
Quality control and fate determination of Hsp90 client proteinsBeyond BRAF: where next for melanoma therapy?Activity of IPI-504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined non-small-cell lung cancer.How do oncoprotein mutations rewire protein-protein interaction networks?Affinity-based proteomics reveal cancer-specific networks coordinated by Hsp90A phase I study of the heat shock protein 90 inhibitor alvespimycin (17-DMAG) given intravenously to patients with advanced solid tumorsSystems biology of cancer: entropy, disorder, and selection-driven evolution to independence, invasion and "swarm intelligence"High-content, high-throughput analysis of cell cycle perturbations induced by the HSP90 inhibitor XL888A melanoma molecular disease modelCanonical and kinase activity-independent mechanisms for extracellular signal-regulated kinase 5 (ERK5) nuclear translocation require dissociation of Hsp90 from the ERK5-Cdc37 complexMapping differential interactomes by affinity purification coupled with data-independent mass spectrometry acquisition.Preclinical studies of celastrol and acetyl isogambogic acid in melanoma.An in silico study of the molecular basis of B-RAF activation and conformational stability.Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel.E3 ubiquitin ligase Cullin-5 modulates multiple molecular and cellular responses to heat shock protein 90 inhibition in human cancer cells.Molecular signature of response and potential pathways related to resistance to the HSP90 inhibitor, 17AAG, in breast cancer.BRAF V600E mutations are common in pleomorphic xanthoastrocytoma: diagnostic and therapeutic implications.Selective BRAFV600E inhibitor PLX4720, requires TRAIL assistance to overcome oncogenic PIK3CA resistance.Safety, efficacy, pharmacokinetics, and pharmacodynamics of the combination of sorafenib and tanespimycinThe E3 ligase CHIP mediates ubiquitination and degradation of mixed-lineage kinase 3A screening assay to identify agents that enhance T-cell recognition of human melanomasAMP-activated kinase (AMPK)-generated signals in malignant melanoma cell growth and survival.HSP90 is a therapeutic target in JAK2-dependent myeloproliferative neoplasms in mice and humansThe HSP90 inhibitor XL888 overcomes BRAF inhibitor resistance mediated through diverse mechanismsProteomic analyses reveal high expression of decorin and endoplasmin (HSP90B1) are associated with breast cancer metastasis and decreased survival.Modulation of melanoma cell phospholipid metabolism in response to heat shock protein 90 inhibition.ATP-competitive inhibitors block protein kinase recruitment to the Hsp90-Cdc37 system.Heat shock protein 90 regulates the expression of Wilms tumor 1 protein in myeloid leukemiasInitial testing (stage 1) of ganetespib, an Hsp90 inhibitor, by the Pediatric Preclinical Testing Program.Activity of the heat shock protein 90 inhibitor ganetespib in melanomaInhibition of ALK, PI3K/MEK, and HSP90 in murine lung adenocarcinoma induced by EML4-ALK fusion oncogeneA first in human, safety, pharmacokinetics, and clinical activity phase I study of once weekly administration of the Hsp90 inhibitor ganetespib (STA-9090) in patients with solid malignancies.Inhibition of HSP90 by AT13387 delays the emergence of resistance to BRAF inhibitors and overcomes resistance to dual BRAF and MEK inhibition in melanoma modelsAn activated mutant BRAF kinase domain is sufficient to induce pilocytic astrocytoma in miceHSP90 inhibitor NVP-AUY922 enhances TRAIL-induced apoptosis by suppressing the JAK2-STAT3-Mcl-1 signal transduction pathway in colorectal cancer cells.Protein signatures correspond to survival outcomes of AJCC stage III melanoma patients.Macrocyclic inhibitors of hsp90The quinone methide aurin is a heat shock response inducer that causes proteotoxic stress and Noxa-dependent apoptosis in malignant melanoma cells.SNX2112, a synthetic heat shock protein 90 inhibitor, has potent antitumor activity against HER kinase-dependent cancers.Phase I trial of 17-allylamino-17-demethoxygeldanamycin in patients with advanced cancer
P2860
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P2860
V600E B-Raf requires the Hsp90 chaperone for stability and is degraded in response to Hsp90 inhibitors
description
2005 nî lūn-bûn
@nan
2005 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@ast
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@en
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@nl
type
label
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@ast
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@en
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@nl
prefLabel
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@ast
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@en
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@nl
P2093
P2860
P356
P1476
V600E B-Raf requires the Hsp90 ...... n response to Hsp90 inhibitors
@en
P2093
O M Grbovic
P Friedlander
P2860
P356
10.1073/PNAS.0609973103
P407
P577
2005-12-21T00:00:00Z