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8 results on '"Dusetti, N.J."'

1. Relevance of biopsy-derived pancreatic organoids in the development of efficient transcriptomic signatures to predict adjuvant chemosensitivity in pancreatic cancer

Author

Nicolle, R., Gayet, O., Bigonnet, M., Roques, J., Chanez, B., Puleo, F., Augustin, J., Emile, J.F., Svrcek, M., Arsenijevic, T., Hammel, P., Rebours, V., Giovannini, M., Grandval, P., Dahan, L., Moutardier, V., Mitry, E., Van Laethem, J.L., Bachet, J.B., Cros, J., Iovanna, J., and Dusetti, N.J.

Published
2022
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2. A transcriptomic signature to predict adjuvant gemcitabine sensitivity in pancreatic adenocarcinoma

Author

Nicolle, R., Gayet, O., Duconseil, P., Vanbrugghe, C., Roques, J., Bigonnet, M., Blum, Y., Elarouci, N., Armenoult, L., Ayadi, M., de Reyniès, A., Puleo, F., Augustin, J., Emile, J.F., Svrcek, M., Arsenijevic, T., Hammel, P., Giovannini, M., Grandval, P., Dahan, L., Moutardier, V., Gilabert, M., Van Laethem, J.L., Bachet, J.B., Cros, J., Iovanna, J., and Dusetti, N.J.

Published
2021
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4. CDK2 and PKA mediated-sequential phosphorylation is critical for p19INK4d function in the DNA damage response

Author

Marazita, M.C., Florencia Ogara, M., Sonzogni, S.V., Martí, M., Dusetti, N.J., Pignataro, O.P., and Cánepa, E.T.

Subjects
ultraviolet radiation, phosphate p 32, DNA Repair, Cell Survival, Ultraviolet Rays, ATM protein, cisplatin, radiation exposure, serine, Humans, cyclin dependent kinase 6, controlled study, genetics, human, Cyclin-Dependent Kinase Inhibitor p19, Phosphorylation, cyclin dependent kinase 2, cell strain HEK293, cyclin dependent kinase 4, cyclic AMP dependent protein kinase, checkpoint kinase 2, Amyloid beta-Peptides, conformational transition, cell nucleus, checkpoint kinase 1, Cyclin-Dependent Kinase 2, drug effect, Cell Cycle, article, DNA, cell line, gene expression regulation, Cyclic AMP-Dependent Protein Kinases, threonine, protein phosphorylation, cyclin dependent kinase inhibitor 2D, Protein Transport, HEK293 Cells, amyloid beta protein, Mutation, DNA damage, point mutation, CDK2 protein, human, metabolism, signal transduction, ATR protein
Abstract

DNA damage triggers a phosphorylation-based signaling cascade known as the DNA damage response. p19INK4d, a member of the INK4 family of CDK4/6 inhibitors, has been reported to participate in the DNA damage response promoting DNA repair and cell survival. Here, we provide mechanistic insight into the activation mechanism of p19INK4d linked to the response to DNA damage. Results showed that p19INK4d becomes phosphorylated following UV radiation, b-amyloid peptide and cisplatin treatments. ATM-Chk2/ATR-Chk1 signaling pathways were found to be differentially involved in p19INK4d phosphorylation depending on the type of DNA damage. Two sequential phosphorylation events at serine 76 and threonine 141 were identified using p19INK4d single-point mutants in metabolic labeling assays with 32P-orthophosphate. CDK2 and PKA were found to participate in p19INK4d phosphorylation process and that they would mediate serine 76 and threonine 141 modifications respectively. Nuclear translocation of p19INK4d induced by DNA damage was shown to be dependent on serine 76 phosphorylation. Most importantly, both phosphorylation sites were found to be crucial for p19INK4d function in DNA repair and cell survival. In contrast, serine 76 and threonine 141 were dispensable for CDK4/6 inhibition highlighting the independence of p19INK4d functions, in agreement with our previous findings. These results constitute the first description of the activation mechanism of p19INK4d in response to genotoxic stress and demonstrate the functional relevance of this activation following DNA damage. © 2012 Marazita et al. Fil:Marazita, M.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Florencia Ogara, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Sonzogni, S.V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Martí, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Dusetti, N.J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pignataro, O.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Cánepa, E.T. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2012

8. The pancreatitis-associated protein is induced by free radicals in AR4-2J cells and confers cell resistance to apoptosis

Author

Ortiz, E.M., Dusetti, N.J., Vasseur, S., Malka, D., Bodeker, H., Dagorn, J., and Iovanna, J.L.

Abstract

Background & Aims: Free radicals are involved in the pathogenesis of acute pancreatitis, during which pancreatitis-associated protein (PAP)-I is overexpressed. We explored whether PAP-I expression could be induced by oxidative stress and whether it could affect apoptosis. Methods: AR4-2J cells were exposed to H"2O"2 or menadione, and PAP-I messenger RNA (mRNA) expression was analyzed by Northern blotting. Results: Maximal expression was observed with 0.1 mmol/L H"2O"2 or with 0.05 mmol/L menadione. Induction was detectable after 12 hours, reached a climax at 18 hours, and then decreased. Pretreatment of the cells with pyrrolidine dithiocarbamate completely abolished PAP-I mRNA induction, suggesting involvement of NF@kB in the signaling pathway. These findings were confirmed in transient transfection assays using a plasmid containing the PAP-I promoter linked to the chloramphenicol acetyltransferase reporter gene. Then the relationship between PAP-I induction and protection against cell damage during oxidative stress was considered. Constitutive PAP-I expression in AR4-2J cells after transfection with PAP-I complementary DNA conferred significant resistance to apoptosis induced by low doses of H"2O"2 but not to necrosis induced by high doses of H"2O"2. Conclusions: These results suggest that during oxidative stress, PAP-I might be part of a mechanism of pancreatic cell protection against apoptosis. GASTROENTEROLOGY 1998;114:808-816

Published
1998
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