Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Jana, Peremartí"'
Publikováno v:
Metallomics. 12:2161-2173
Arsenic induces oncogenic effects activating stress-related signalling pathways. This can result in the over-activation of the AP-1 protein, specifically its FRA1 component. FRA1 is a transcription factor frequently overexpressed in epithelial tumors
Publikováno v:
Metallomics : integrated biometal science. 12(12)
Arsenic induces oncogenic effects activating stress-related signalling pathways. This can result in the over-activation of the AP-1 protein, specifically its FRA1 component. FRA1 is a transcription factor frequently overexpressed in epithelial tumors
Autor:
J C States, Laila Al-Eryani, Samantha F. Jenkins, Chendil Damodaran, Ashish Tyagi, Sabine Waigel, Jana Peremartí
Publikováno v:
Toxicological Sciences. 162:645-654
Arsenic is a widely distributed toxic natural element. Chronic arsenic ingestion causes several cancers, especially skin cancer. Arsenic-induced cancer mechanisms are not well defined, but several studies indicate that mutation is not the driving for
Publikováno v:
Toxicology and Applied Pharmacology. 409:115303
DNA damage plays a crucial role in the transforming potential of the human carcinogen arsenic. The arsenic biotransformation enzyme AS3MT is known to participate in the generation of ROS after arsenic exposure, whereas MTH1 sanitizes oxidized dNTP po
Publikováno v:
Archives of Toxicology. 90:1893-1905
Chronic exposure to arsenic is known to increase the incidence of cancer in humans. Our previous work demonstrated that environmentally relevant arsenic exposures generate an accelerated accumulation of pre-carcinogen 8-OH-dG DNA lesions under Ogg1-d
Publikováno v:
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 779:144-151
Inorganic arsenic (i-As) is a genotoxic and carcinogenic environmental contaminant known to affect millions of people worldwide. Our previous work demonstrated that chronic sub-toxic i-As concentrations were able to induce biologically significant le
Publikováno v:
Toxicological Sciences. 142:93-104
Chronic arsenic exposure is known to enhance the genotoxicity/carcinogenicity of other DNA-damaging agents by inhibiting DNA repair activities. Interference with nucleotide excision repair and base excision repair are well documented, but interaction