Search

Your search keyword '"Saltini, Giuliana"' showing total 9 results
Start Over Author "Saltini, Giuliana"
9 results on '"Saltini, Giuliana"'

4. A novel polymorphism in SEL1L confers susceptibility to Alzheimer's disease

Author

Saltini, Giuliana, primary, Dominici, Roberto, additional, Lovati, Carlo, additional, Cattaneo, Monica, additional, Michelini, Stefania, additional, Malferrari, Giulia, additional, Caprera, Andrea, additional, Milanesi, Luciano, additional, Finazzi, Dario, additional, Bertora, Pierluigi, additional, Scarpini, Elio, additional, Galimberti, Daniela, additional, Venturelli, Eliana, additional, Musicco, Massimo, additional, Adorni, Fulvio, additional, Mariani, Claudio, additional, and Biunno, Ida, additional

Published
2006
Full Text
View/download PDF

6. Protozoan and Hepatitis B Virus DNA Detection in Human Samples

Author

Biagiotti, Laura, primary, Gramegna, Maurizio, additional, Valisi, Massimiliano, additional, Madama, Stefania, additional, Saltini, Giuliana, additional, Dominici, Roberto, additional, Malferrari, Giulia, additional, Monferini, Eugenia, additional, Proverbio, Maria Carla, additional, De Blasio, Pasquale, additional, and Biunno, Ida, additional

Published
2004
Full Text
View/download PDF

8. RNA-Mediated Interference Indicates that SEL1L Plays a Role in Pancreatic β-Cell Growth.

Author

Diaferia, Giuseppe, Cattaneo, Monica, Saltini, Giuliana, Proverbio, Maria Carla, Monferini, Eugenia, Malferrari, Giulia, Albertini, Alberto, and Biunno, Ida

Subjects
PANCREATIC beta cells, PANCREAS, GROWTH factors, PROTEINS, ENDOPLASMIC reticulum, CELL proliferation, IMMUNE response
Abstract

The specificity of SEL1L expression and promoter activity for the pancreatic cell population, its chromosomal location, as well as its similarities to the yeast Hrd3p protein, a component of HRD complex which is responsible for endoplasmic reticulum (ER)-associated degradation of numerous ER-resident proteins, prompted us to study its effects on beta cell function. In this study we show that lowering SEL1L expression, by using the short interfering RNAs technology as well as antisense transfection, resulted in severe perturbation of βTC-3 growth and metabolic activity. We hypothesize that SEL1L may exert its function by protecting the cells from ER stress and could counteract immune responses. [ABSTRACT FROM AUTHOR]

Published
2004
Full Text
View/download PDF

9. Purification of the Aldehyde Oxidase Homolog 1 (AOH1) Protein and Cloning of the AOH1and Aldehyde Oxidase Homolog 2 (AOH2) Genes

Author

Terao, Mineko, Kurosaki, Mami, Marini, Massimiliano, Vanoni, Maria Antonietta, Saltini, Giuliana, Bonetto, Valentina, Bastone, Antonio, Federico, Concetta, Saccone, Salvatore, Fanelli, Roberto, Salmona, Mario, and Garattini, Enrico

Abstract

We report the cloning of the AOH1andAOH2genes, which encode two novel mammalian molybdo-flavoproteins. We have purified the AOH1 protein to homogeneity in its catalytically active form from mouse liver. Twenty tryptic peptides, identified or directly sequenced by mass spectrometry, confirm the primary structure of the polypeptide deduced from theAOH1gene. The enzyme contains one molecule of FAD, one atom of molybdenum, and four atoms of iron per subunit and shows spectroscopic features similar to those of the prototypic molybdo-flavoprotein xanthine oxidoreductase. The AOH1andAOH2genes are 98 and 60 kilobases long, respectively, and consist of 35 coding exons. The AOH1gene has the potential to transcribe an extra leader non-coding exon, which is located downstream of exon 26, and is transcribed in the opposite orientation relative to all the other exons. AOH1and AOH2map to chromosome 1 in close proximity to each other and to the aldehyde oxidase gene, forming a molybdo-flavoenzyme gene cluster. Conservation in the position of exon/intron junctions among the mouseAOH1, AOH2, aldehyde oxidase, and xanthine oxidoreductase loci indicates that these genes are derived from the duplication of an ancestral precursor.

Published
2001
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results