Laura del Senno

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This study addresses the hypothesis that transfection of oligonucleotide mimicking a negative regulatory sequence of promoter C of estrogen receptor alpha (ERα) gene is sufficient for its re-expression in ER-negative human cancer cell lines. Even if the negative transcription regulator subtracted by the transcription factor decoy is not yet been identified,(More)
Transcriptional activity of human estrogen receptor (hER) gene was modulated by competition with double-stranded PCR-generated DNA fragments (decoys) that contain 5′ upstream sequences of the hER gene. Two DNA fragments belonging to the P1 canonical promoter and the P3 distal promoter, 120 and 102 bp in size respectively, were produced by PCR and directly(More)
In autosomal dominant polycystic kidney disease (ADPKD), renal cyst development and enlargement, as well as cell growth, are associated with alterations in several pathways, including cAMP and activator protein 1 (AP1) signalling. However, the precise mechanism by which these molecules stimulate cell proliferation is not yet fully understood. We now show by(More)
Autosomal recessive polycystic kidney disease (ARPKD) is caused by mutations in PKHD1, a gene encoding fibrocystin/polyductin (FC1), a membrane-associated receptor-like protein involved in the regulation of tubular cell adhesion, proliferation and apoptosis. Although it is generally accepted that apoptosis is implicated in ARPKD, the question of whether(More)
Polycystin-1 (PC1), the PKD1 gene product, is a membrane receptor which regulates many cell functions, including cell proliferation and apoptosis, both typically increased in cyst lining cells in autosomal dominant polycystic kidney disease. Here we show that PC1 upregulates the NF-jB signalling pathway in kidney cells to prevent cell death. Human embryonic(More)
This study addresses the hypothesis that transfection of oligonucleotide mimicking a negative regulatory sequence of promoter C of estrogen receptor alpha (ER alpha) gene is sufficient for its re-expression in ER-negative human cancer cell lines. Even if the negative transcription regulator subtracted by the transcription factor decoy is not yet been(More)
Haemophilia B is an inherited X linked disease ' caused by a heterogeneous2 functional deficiency of factor IX, a glycoprotein involved in the intrinsic pathway of blood coagulation.3 The recent cloning of DNA fragments coding for human factor IX4 has allowed the identification of a genetic lesion in haemophilia B9 1" and the detection of an intragenic(More)
Six P3-thalassaemic patients from the Po river delta region have been studied. Using synthetic oligonucleotides as specific hybridisation probes, the ,B+ IVS I mutation (G->A at position 108) was demonstrated. This lesion and the enzyme polymorphism pattern in the subjects examined are the same as have been described for other Mediterranean +thalassaemias.(More)
By analyzing c-myc specific fragments from white blood cell DNAs of 98 gastric cancer patients and 46 control subjects, we observed 6 unexpected patterns due to presence of a variant c-myc gene in addition to the normal gene. Restriction enzyme mapping indicated that the variant c-myc gene was the result of a 5′ deletion including the first exon and part of(More)
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