Persistent induction of c-fos and c-jun expression by asbestos - Wikidata - awgldk - TriplyDB

Persistent induction of c-fos and c-jun expression by asbestos

Persistent induction of c-fos and c-jun expression by asbestos

http://www.wikidata.org/entity/Q36236354

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Testing of fibrous particles: short-term assays and strategies - report of an ILSI Risk Science Institute working group Single- and multi-wall carbon nanotubes versus asbestos: are the carbon nanotubes a new health risk to humans?Oxidative and molecular interactions of multi-wall carbon nanotubes (MWCNT) in normal and malignant human mesothelial cells Raw single-wall carbon nanotubes induce oxidative stress and activate MAPKs, AP-1, NF-kappa B, and Akt in normal and malignant human mesothelial cells Asbestos induces nuclear factor kappa B (NF-kappa B) DNA-binding activity and NF-kappa B-dependent gene expression in tracheal epithelial cells Cell signaling pathways elicited by asbestos Modulation of mitochondrial gene expression in pulmonary epithelial cells exposed to oxidants Crocidolite induces cell transformation and p53 gene mutation in BALB/c-3T3 cells Differences in gene expression and cytokine production by crystalline vs. amorphous silica in human lung epithelial cells A protein kinase Cdelta-dependent protein kinase D pathway modulates ERK1/2 and JNK1/2 phosphorylation and Bim-associated apoptosis by asbestos Oxidants and signaling by mitogen-activated protein kinases in lung epithelium Possible role of lipid peroxidation in the induction of NF-kappa B and AP-1 in RFL-6 cells by crocidolite asbestos: evidence following protection by vitamin E Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos Proteomic profiling change during the early development of silicosis disease Cellular and molecular parameters of mesothelioma Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways Biopersistence and potential adverse health impacts of fibrous nanomaterials: what have we learned from asbestos?Increased epidermal growth factor-receptor protein in a human mesothelial cell line in response to long asbestos fibers Up-regulated expression of transforming growth factor-alpha in the bronchiolar-alveolar duct regions of asbestos-exposed rats Multiple cis-elements mediate the transcriptional activation of human fra-1 by 12-O-tetradecanoylphorbol-13-acetate in bronchial epithelial cells Asbestos induces mitochondrial DNA damage and dysfunction linked to the development of apoptosis.Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines.Mechanisms of asbestos carcinogenesis and toxicity: the amphibole hypothesis revisited Asbestos, chromosomal deletions, and tumor suppressor gene alterations in human malignant mesothelioma.Emerging roles of ATF2 and the dynamic AP1 network in cancer.Combined effects of asbestos and cigarette smoke on the development of lung adenocarcinoma: different carcinogens may cause different genomic changes.Identification of novel candidate oncogenes and tumor suppressors in malignant pleural mesothelioma using large-scale transcriptional profiling.p53, Cip1, and Gadd153 expression following treatment of A549 cells with natural and man-made vitreous fibers.Crocidolite asbestos induces apoptosis of pleural mesothelial cells: role of reactive oxygen species and poly(ADP-ribosyl) polymerase Oxygen radicals and asbestos-mediated disease Oxygen radicals and asbestos carcinogenesis.Vitronectin enhances internalization of crocidolite asbestos by rabbit pleural mesothelial cells via the integrin alpha v beta 5 Patterns of inflammation, cell proliferation, and related gene expression in lung after inhalation of chrysotile asbestos Molecular biology of malignant mesothelioma.Asbestos induces apoptosis of human and rabbit pleural mesothelial cells via reactive oxygen species.Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos cocarcinogenicity.Induction of tunica vaginalis mesotheliomas in rats by xenobiotics.Dielectric changes in membrane properties and cell interiors of human mesothelial cells in vitro after crocidolite asbestos exposure.Blocking of ERK1 and ERK2 sensitizes human mesothelioma cells to doxorubicin.

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P2860

Persistent induction of c-fos and c-jun expression by asbestos

http://www.wikidata.org/entity/Q36236354

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1993 nî lūn-bûn

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1993年の論文

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1993年学术文章

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1993年学术文章

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1993年学术文章

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1993年学术文章

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1993年学术文章

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1993年學術文章

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1993年學術文章

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1993年學術文章

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Persistent induction of c-fos and c-jun expression by asbestos

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Persistent induction of c-fos and c-jun expression by asbestos

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Persistent induction of c-fos and c-jun expression by asbestos

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Persistent induction of c-fos and c-jun expression by asbestos

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

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Persistent induction of c-fos and c-jun expression by asbestos

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P2093

B T Mossman

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N H Heintz

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Y M Janssen

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P2860

The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation

Hydrolysis of inositol phospholipids precedes cellular proliferation in asbestos-stimulated tracheobronchial epithelial cells

Correlation of in vitro genotoxicity and oncogenicity induced by radiation and asbestos fibres

The pathogenicity of long versus short fibre samples of amosite asbestos administered to rats by inhalation and intraperitoneal injection.

Biphasic increase in c-jun mRNA is required for induction of AP-1-mediated gene transcription: differential effects of muscarinic and thrombin receptor activation

Asbestos-associated chromosomal changes in human mesothelial cells.

Nuclear proto-oncogenes fos and jun.

Too many rodent carcinogens: mitogenesis increases mutagenesis.

The product of a fos-related gene, fra-1, binds cooperatively to the AP-1 site with Jun: transcription factor AP-1 is comprised of multiple protein complexes.

Increased cell division as a cause of human cancer.

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3299-3303

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