High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer. - Wikidata - awgldk - TriplyDB

High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer.

High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer.

http://www.wikidata.org/entity/Q35546764

about

Englerin A stimulates PKCθ to inhibit insulin signaling and to simultaneously activate HSF1: pharmacologically induced synthetic lethality Contribution of the Type II Chaperonin, TRiC/CCT, to Oncogenesis Pleiotropic role of HSF1 in neoplastic transformation Heat-shock factor 2 is a suppressor of prostate cancer invasion.IER5 generates a novel hypo-phosphorylated active form of HSF1 and contributes to tumorigenesis mTOR is essential for the proteotoxic stress response, HSF1 activation and heat shock protein synthesis Uncoupling Stress-Inducible Phosphorylation of Heat Shock Factor 1 from Its Activation Heat shock proteins and heat shock factor 1 in carcinogenesis and tumor development: an update Photothermal therapy of glioblastoma multiforme using multiwalled carbon nanotubes optimized for diffusion in extracellular space Transportable, Chemical Genetic Methodology for the Small Molecule-Mediated Inhibition of Heat Shock Factor 1 Expression of HSF2 decreases in mitosis to enable stress-inducible transcription and cell survival.Overexpression of heat-shock factor 1 is associated with a poor prognosis in esophageal squamous cell carcinoma HER2/ErbB2 activates HSF1 and thereby controls HSP90 clients including MIF in HER2-overexpressing breast cancer Integrin-linked kinase modulates longevity and thermotolerance in C. elegans through neuronal control of HSF-1.IER5 as a promising predictive marker promotes irradiation-induced apoptosis in cervical cancer tissues from patients undergoing chemoradiotherapy High level of HSF1 associates with aggressive endometrial carcinoma and suggests potential for HSP90 inhibitors.Bromodomain factors of BET family are new essential actors of pericentric heterochromatin transcriptional activation in response to heat shock Proteotoxicity is not the reason for the dependence of cancer cells on the major chaperone Hsp70 Akt phosphorylates and activates HSF-1 independent of heat shock, leading to Slug overexpression and epithelial-mesenchymal transition (EMT) of HER2-overexpressing breast cancer cells.Quantitative proteomics reveals that Hsp90 inhibition preferentially targets kinases and the DNA damage response.HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers.Small molecule activators of the heat shock response: chemical properties, molecular targets, and therapeutic promise.The SIRT1 modulators AROS and DBC1 regulate HSF1 activity and the heat shock response.The reprogramming of tumor stroma by HSF1 is a potent enabler of malignancy.HSF1 regulation of β-catenin in mammary cancer cells through control of HuR/elavL1 expression.Overexpression of Heat Shock Transcription Factor 1 enhances the resistance of melanoma cells to doxorubicin and paclitaxel.Heat shock factor 1 confers resistance to Hsp90 inhibitors through p62/SQSTM1 expression and promotion of autophagic flux HSF1 functions as a transcription regulator for Dp71 expression.FBXW7 modulates cellular stress response and metastatic potential through HSF1 post-translational modification.Mutant p53 - Heat Shock Response Oncogenic Cooperation: A New Mechanism of Cancer Cell Survival.The crossroads between cancer stem cells and aging.The unpredictability of prolonged activation of stress response pathways.Using the heat-shock response to discover anticancer compounds that target protein homeostasis.Molecular chaperones in mammary cancer growth and breast tumor therapy Heat shock factor 1 induces cancer stem cell phenotype in breast cancer cell lines Heat shock factor-1 knockout induces multidrug resistance gene, MDR1b, and enhances P-glycoprotein (ABCB1)-based drug extrusion in the heart.Mitochondrial Respiratory Dysfunction Induces Claudin-1 Expression via Reactive Oxygen Species-mediated Heat Shock Factor 1 Activation, Leading to Hepatoma Cell Invasiveness.RIPK1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy.Proteotoxic stress of cancer: implication of the heat-shock response in oncogenesis.Higher heat shock factor 1 expression in tumor stroma predicts poor prognosis in esophageal squamous cell carcinoma patients

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High levels of nuclear heat-shock factor 1 (HSF1) are associated with poor prognosis in breast cancer.

http://www.wikidata.org/entity/Q35546764

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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Proceedings of the National Academy of Sciences of the United States of America

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High levels of nuclear heat-sh ...... or prognosis in breast cancer.

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Laura C Collins

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Nancy U Lin

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Rong Hu

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Rulla M Tamimi

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Sandro Santagata

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Stuart J Schnitt

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Susan E Hankinson

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Tan A Ince

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P2860

Chromatin landscape dictates HSF binding to target DNA elements

Proinvasion metastasis drivers in early-stage melanoma are oncogenes.

Molecular cloning and expression of a human heat shock factor, HSF1

Heat shock factor 1 is a powerful multifaceted modifier of carcinogenesis

Aneuploidy affects proliferation and spontaneous immortalization in mammalian cells

A gene-expression signature as a predictor of survival in breast cancer

Isolation of the gene encoding the S. cerevisiae heat shock transcription factor.

A naturally occurring MTA1 variant sequesters oestrogen receptor-alpha in the cytoplasm

Targeting the dynamic HSP90 complex in cancer

Riluzole increases the amount of latent HSF1 for an amplified heat shock response and cytoprotection

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10.1073/PNAS.1115031108

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45

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108

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Susan Lindquist

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