NAD(P)H:Quinone oxidoreductase activity is the principal determinant of beta-lapachone cytotoxicity. - Wikidata - wikimedia - TriplyDB

NAD(P)H:Quinone oxidoreductase activity is the principal determinant of beta-lapachone cytotoxicity.

NAD(P)H:Quinone oxidoreductase activity is the principal determinant of beta-lapachone cytotoxicity.

http://www.wikidata.org/entity/Q40899393

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Potential mechanism of phytochemical-induced apoptosis in human prostate adenocarcinoma cells: Therapeutic synergy in genistein and beta-lapachone combination treatment NAD(P)H:quinone oxidoreductase 1 (NQO1) in the sensitivity and resistance to antitumor quinones Modulating endogenous NQO1 levels identifies key regulatory mechanisms of action of β-lapachone for pancreatic cancer therapy.Beta-lapachone suppresses radiation-induced activation of nuclear factor-kappaB Redox regulation of mitochondrial function Mitochondrial targeted β-lapachone induces mitochondrial dysfunction and catastrophic vacuolization in cancer cells A chemical genetic screen for modulators of asymmetrical 2,2'-dimeric naphthoquinones cytotoxicity in yeast Distinct genes related to drug response identified in ER positive and ER negative breast cancer cell lines Molecular resistance fingerprint of pemetrexed and platinum in a long-term survivor of mesothelioma Sulindac compounds facilitate the cytotoxicity of β-lapachone by up-regulation of NAD(P)H quinone oxidoreductase in human lung cancer cells Features of idebenone and related short-chain quinones that rescue ATP levels under conditions of impaired mitochondrial complex I NQO1-dependent redox cycling of idebenone: effects on cellular redox potential and energy levels Nuclear clusterin/XIP8, an x-ray-induced Ku70-binding protein that signals cell death.β-lapachone significantly increases the effect of ionizing radiation to cause mitochondrial apoptosis via JNK activation in cancer cells.E1B and E4 oncoproteins of adenovirus antagonize the effect of apoptosis inducing factor Intratumoral delivery of beta-lapachone via polymer implants for prostate cancer therapy Tumor-selective, futile redox cycle-induced bystander effects elicited by NQO1 bioactivatable radiosensitizing drugs in triple-negative breast cancers.Beta-lapachone micellar nanotherapeutics for non-small cell lung cancer therapy.Endoplasmic reticulum stress-induced JNK activation is a critical event leading to mitochondria-mediated cell death caused by β-lapachone treatment.β-Lapachone induces heart morphogenetic and functional defects by promoting the death of erythrocytes and the endocardium in zebrafish embryos Prodrug strategy to achieve lyophilizable, high drug loading micelle formulations through diester derivatives of β-Lapachone.Beta-lapachone, a modulator of NAD metabolism, prevents health declines in aged mice.Regulation of p53 stability and p53-dependent apoptosis by NADH quinone oxidoreductase 1 Selective killing of cancer cells by beta -lapachone: direct checkpoint activation as a strategy against cancer.The curcuminoid CLEFMA selectively induces cell death in H441 lung adenocarcinoma cells via oxidative stress.Photophysics and photochemistry of the β-lapachone derived diphenyldihydrodioxin: generation and characterization of its cation radical.SoNar, a Highly Responsive NAD+/NADH Sensor, Allows High-Throughput Metabolic Screening of Anti-tumor Agents.RETRACTED: NAD(P)H:quinone oxidoreductase 1 protects lungs from oxidant-induced emphysema in mice.An NQO1- and PARP-1-mediated cell death pathway induced in non-small-cell lung cancer cells by beta-lapachone.Upregulation of NAD(P)H:quinone oxidoreductase by radiation potentiates the effect of bioreductive beta-lapachone on cancer cells.Quinone reductases multitasking in the metabolic world.Beta-lapachone-containing PEG-PLA polymer micelles as novel nanotherapeutics against NQO1-overexpressing tumor cells Targeting glutamine metabolism sensitizes pancreatic cancer to PARP-driven metabolic catastrophe induced by ß-lapachone Efficacious fluorescence turn-on probe for high-contrast imaging of human cells overexpressing quinone reductase activity.Tumor-selective use of DNA base excision repair inhibition in pancreatic cancer using the NQO1 bioactivatable drug, β-lapachone.Fibulin-5 Blocks Microenvironmental ROS in Pancreatic Cancer.PRX1 knockdown potentiates vitamin K3 toxicity in cancer cells: a potential new therapeutic perspective for an old drug.Depleting Tumor-NQO1 Potentiates Anoikis and Inhibits Growth of NSCLC.Nuclear ULK1 promotes cell death in response to oxidative stress through PARP1 Superparamagnetic iron oxide nanoparticles: amplifying ROS stress to improve anticancer drug efficacy.

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P2860

NAD(P)H:Quinone oxidoreductase activity is the principal determinant of beta-lapachone cytotoxicity.

http://www.wikidata.org/entity/Q40899393

description

2000 nî lūn-bûn

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2000年の論文

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2000年学术文章

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2000年学术文章

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2000年学术文章

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2000年学术文章

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2000年学术文章

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2000年學術文章

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2000年學術文章

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2000年學術文章

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name

NAD(P)H:Quinone oxidoreductase ...... f beta-lapachone cytotoxicity.

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type

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NAD(P)H:Quinone oxidoreductase ...... f beta-lapachone cytotoxicity.

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NAD(P)H:Quinone oxidoreductase ...... f beta-lapachone cytotoxicity.

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NAD(P)H:Quinone oxidoreductase ...... f beta-lapachone cytotoxicity.

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P2093

C Tagliarino

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D A Boothman

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D Siegel

http://www.w3.org/2001/XMLSchema#string

J J Pink

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M E Varnes

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S M Planchon

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P2860

DNA damage-inducible transcripts in mammalian cells

Unexpected genetic and structural relationships of a long-forgotten flavoenzyme to NAD(P)H:quinone reductase (DT-diaphorase)

Quinone reductase inhibitors block SAPK/JNK and NFkappaB pathways and potentiate apoptosis

Inhibition of radiation-induced neoplastic transformation by beta-lapachone

DT-diaphorase and cancer chemotherapy.

Irreversible loss of the oestrogen receptor in T47D breast cancer cells following prolonged oestrogen deprivation

DT-diaphorase and cytochrome B5 reductase in human lung and breast tumours

Isolation of x-ray-inducible transcripts from radioresistant human melanoma cells.

Proteolytic cleavage of human p53 by calpain: a potential regulator of protein stability.

DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways.

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