Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling. - Wikidata - wikimedia - TriplyDB

Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling.

Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling.

http://www.wikidata.org/entity/Q36423404

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Dioxins and cardiovascular disease mortality Dual localization of glutathione S-transferase in the cytosol and mitochondria: implications in oxidative stress, toxicity and disease Mitochondrial DNA damage and its consequences for mitochondrial gene expression The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis Exactly the same but different: promiscuity and diversity in the molecular mechanisms of action of the aryl hydrocarbon (dioxin) receptor Dynamic zebrafish interactome reveals transcriptional mechanisms of dioxin toxicity Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine-disrupting chemicals and biophysical laws TCDD promotes lung tumors via attenuation of apoptosis through activation of the Akt and ERK1/2 signaling pathways.Chloramphenicol causes mitochondrial stress, decreases ATP biosynthesis, induces matrix metalloproteinase-13 expression, and solid-tumor cell invasion.Moesin is a biomarker for the assessment of genotoxic carcinogens in mouse lymphoma.Strong associations between the pesticide hexachlorocyclohexane and type 2 diabetes in Saudi adults.Association between type 2 diabetes and exposure to persistent organic pollutants.DDT and its metabolites are linked to increased risk of type 2 diabetes among Saudi adults: a cross-sectional study.Circulating persistent organic pollutants and body fat distribution: Evidence from NHANES 1999-2004.2,3,7,8-Tetrachlorodibenzo-p-dioxin-mediated production of reactive oxygen species is an essential step in the mechanism of action to accelerate human keratinocyte differentiation.Mitochondria as a target of environmental toxicants.Ah Receptor Activation by Dioxin Disrupts Activin, BMP, and WNT Signals During the Early Differentiation of Mouse Embryonic Stem Cells and Inhibits Cardiomyocyte Functions Mitochondrial retrograde signaling at the crossroads of tumor bioenergetics, genetics and epigenetics.Heterogeneous nuclear ribonucleoprotein A2 is a common transcriptional coactivator in the nuclear transcription response to mitochondrial respiratory stress.Mutations in mitochondrial DNA polymerase-gamma promote breast tumorigenesis Identification of EBP50 as a specific biomarker for carcinogens via the analysis of mouse lymphoma cellular proteome.Implications of mitochondrial DNA mutations and mitochondrial dysfunction in tumorigenesis.Fish oil rich in eicosapentaenoic acid protects against oxidative stress-related renal dysfunction induced by TCDD in Wistar rats.Dioxin toxicity, aryl hydrocarbon receptor signaling, and apoptosis-persistent pollutants affect programmed cell death.The use of α-fetoprotein for the delivery of cytotoxic payloads to cancer cells.Classical and Novel TSPO Ligands for the Mitochondrial TSPO Can Modulate Nuclear Gene Expression: Implications for Mitochondrial Retrograde Signaling.Mitochondrial-targeted aryl hydrocarbon receptor and the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin on cellular respiration and the mitochondrial proteome.Mitochondrial dysfunction and mitochondrial dynamics-The cancer connection.Release of targeted p53 from the mitochondrion as an early signal during mitochondrial dysfunction.Role of calcineurin, hnRNPA2 and Akt in mitochondrial respiratory stress-mediated transcription activation of nuclear gene targets.Synergistic cellular effects including mitochondrial destabilization, autophagy and apoptosis following low-level exposure to a mixture of lipophilic persistent organic pollutants.A distinctive physiological role for IkappaBbeta in the propagation of mitochondrial respiratory stress signaling.β-Naphthoflavone-Induced Mitochondrial Respiratory Damage in Cyp1 Knockout Mouse and in Cell Culture Systems: Attenuation by Resveratrol Treatment.Metabolomic analysis of liver and skeletal muscle tissues in C57BL/6J and DBA/2J mice exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.Dioxin-sensitive proteins in differentiating osteoblasts: effects on bone formation in vitro.Actein alleviates 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated cellular dysfunction in osteoblastic MC3T3-E1 cells.Early Life Exposure to Low Levels of AHR Agonist PCB126 (3,3',4,4',5-Pentachlorobiphenyl) Reprograms Gene Expression in Adult Brain.From dioxin to dioxin congeners: understanding the differences in hydrophobic aggregation in water and absorption into lipid membranes by means of atomistic simulations.

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P2860

Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling.

http://www.wikidata.org/entity/Q36423404

description

2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Dioxin-mediated tumor progress ...... a-to-nucleus stress signaling.

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Gopa Biswas

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Hindupur K Anandatheerthavarada

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Narayan G Avadhani

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Satish Srinivasan

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P2860

Targets for dioxin: genes for plasminogen activator inhibitor-2 and interleukin-1 beta

2,3,7,8-Tetrachlorodibenzo-p-dioxin-dependent regulation of transforming growth factors-alpha and -beta 2 expression in a human keratinocyte cell line involves both transcriptional and post-transcriptional control

Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion

Activation of transcription factors activator protein-1 and nuclear factor-kappaB by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Dioxin induces expression of c-fos and c-jun proto-oncogenes and a large increase in transcription factor AP-1

A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine

2,3,7,8-tetrachlorodibenzo-p-dioxin and related halogenated aromatic hydrocarbons: examination of the mechanism of toxicity

Antisense RNA inhibition of cathepsin L expression reduces tumorigenicity of malignant cells.

Putative link between transcriptional regulation of IgM expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin and the aryl hydrocarbon receptor/dioxin-responsive enhancer signaling pathway.

CREB activation induced by mitochondrial dysfunction is a new signaling pathway that impairs cell proliferation.

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