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1.
Int J Mol Sci ; 19(2)2018 Jan 31.
Article in English | MEDLINE | ID: mdl-29385075

ABSTRACT

Persistent cervical infection with high-risk human papillomaviruses (hrHPVs) is a necessary, but not sufficient, condition for the development of cervical cancer. Therefore, there are other co-factors facilitating the hrHPV carcinogenic process, one of which is smoking. To assess the effect of smoking on high-risk (hr) HPV DNA positivity and on the expression of HPV E7 oncoprotein, as a surrogate of persistent hrHPV infection, we used data from women recruited for the PIPAVIR project, which examined the role of E7 protein detection in cervical cancer screening. Women were tested for hrHPV DNA, using Multiplex Genotyping (MPG), and E7 protein, using a novel sandwich ELISA method, and gave information on their smoking habits. Among 1473 women, hrHPV prevalence was 19.1%. The odds ratio (OR) for hrHPV positivity of smokers compared to non-smokers was 1.785 (95% confidence intervals (CI): 1.365-2.332, p < 0.001). The ORs for E7 positivity, concerning hrHPV positive women, ranged from 0.720 to 1.360 depending on the E7 detection assay used, but this was not statistically significant. Smoking increases the probability of hrHPV infection, and smoking intensity is positively associated to this increase. Smoking is not related to an increased probability of E7 protein positivity for hrHPV positive women.


Subject(s)
Cigarette Smoking/adverse effects , Papillomavirus E7 Proteins/analysis , Papillomavirus Infections/metabolism , Uterine Cervical Neoplasms/etiology , Adult , Female , Humans , Middle Aged , Papillomavirus Infections/complications , Papillomavirus Infections/epidemiology , Papillomavirus Infections/etiology , Risk Factors
2.
J Cell Biol ; 216(12): 4007-4026, 2017 12 04.
Article in English | MEDLINE | ID: mdl-29030393

ABSTRACT

Proteins disabled in the cancer-prone disorder Fanconi anemia (FA) ensure the maintenance of chromosomal stability during DNA replication. FA proteins regulate replication dynamics, coordinate replication-coupled repair of interstrand DNA cross-links, and mitigate conflicts between replication and transcription. Here we show that FANCI and FANCD2 associate with splicing factor 3B1 (SF3B1), a key spliceosomal protein of the U2 small nuclear ribonucleoprotein (U2 snRNP). FANCI is in close proximity to SF3B1 in the nucleoplasm of interphase and mitotic cells. Furthermore, we find that DNA replication stress induces the release of SF3B1 from nuclear speckles in a manner that depends on FANCI and on the activity of the checkpoint kinase ATR. In chromatin, both FANCD2 and FANCI associate with SF3B1, prevent accumulation of postcatalytic intron lariats, and contribute to the timely eviction of splicing factors. We propose that FANCD2 and FANCI contribute to the organization of functional domains in chromatin, ensuring the coordination of DNA replication and cotranscriptional processes.


Subject(s)
DNA Replication , Fanconi Anemia Complementation Group D2 Protein/genetics , Fanconi Anemia Complementation Group Proteins/genetics , Fanconi Anemia/genetics , Phosphoproteins/genetics , RNA Splicing Factors/genetics , Transcription, Genetic , Ataxia Telangiectasia Mutated Proteins/genetics , Ataxia Telangiectasia Mutated Proteins/metabolism , Cell Line, Tumor , Chromatin/metabolism , Chromatin/ultrastructure , Fanconi Anemia/metabolism , Fanconi Anemia/pathology , Fanconi Anemia Complementation Group D2 Protein/metabolism , Fanconi Anemia Complementation Group Proteins/metabolism , Fibroblasts/metabolism , Fibroblasts/pathology , Genes, Reporter , HEK293 Cells , HeLa Cells , Humans , Mitosis , Oligopeptides/genetics , Oligopeptides/metabolism , Osteoblasts/metabolism , Osteoblasts/pathology , Phosphoproteins/metabolism , Protein Binding , RNA Splicing Factors/metabolism , Ribonucleoprotein, U2 Small Nuclear/genetics , Ribonucleoprotein, U2 Small Nuclear/metabolism , Spliceosomes/metabolism , Spliceosomes/ultrastructure
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