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32 results on '"Nappi, Filomena"'

1. List of contributors

Author

Adamik, Juraj, primary, Aurisicchio, Luigi, additional, Bell, John C., additional, Bourgeois-Daigneault, Marie-Claude, additional, Butterfield, Lisa H., additional, Cerullo, Vincenzo, additional, Chiang, Cheryl L.-L., additional, Ciliberto, Gennaro, additional, Conforti, Antonella, additional, Finn, Olivera J., additional, Galli, Maria Cristina, additional, Hadrup, Sine Reker, additional, Hamilton, Duane H., additional, Hawthorne, Jenci, additional, Himuro, Hidetomo, additional, Jacqueline, Camille, additional, Jochems, Caroline, additional, Kadivar, Mohammad, additional, Kandalaft, Lana E., additional, Melief, Cornelis J.M., additional, Munson, Paul V., additional, Nappi, Filomena, additional, Palombo, Fabio, additional, Rammensee, Hans-Georg, additional, Sasada, Tetsuro, additional, Schlom, Jeffrey, additional, Shirwan, Haval, additional, Tagliamonte, Maria, additional, van der Gracht, Esmé T.I., additional, Wiekmeijer, Anna-Sophia, additional, Ylösmäki, Erkko, additional, and Yolcu, Esma, additional

Published
2022
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3. List of Contributors

Author

Allickson, Julie G., primary, Amado, Rafael G., additional, Azam, Usman, additional, Barry, Frank, additional, Bilbao, Irene Aldecoa, additional, Binder, Gwendolyn K., additional, Black, Justin L., additional, Blumer, Karin, additional, Brandon, Eugene P., additional, Brindley, David A., additional, Burns, William Murray, additional, Capone, Francesca, additional, Carmona, Guillaume, additional, Chaffman, Michael, additional, Chou, William, additional, Cui, Zhanfeng, additional, D’Amour, Kevin A., additional, Dowden, Nathan J., additional, Eschgfaeller, Bernd, additional, Faulkner, Eric, additional, Galli, Maria Cristina, additional, Goshima, Yoshio, additional, Haggarty, Stephen J., additional, Halioua-Haubold, Celine-Lea, additional, Harrington-Smith, Kristen, additional, Hickerson, Darren, additional, Ho, William, additional, Hyllner, Johan, additional, Iyer, Natasha, additional, Jansen, Marieke, additional, Jousseaume, Etienne, additional, Kili, Sven, additional, Konski, Antoinette F., additional, Lamb, Lawrence S., additional, Lam, Ching, additional, Lim, Jaeseung, additional, Lo, Chi, additional, Malcolm, Thomas, additional, Martinez-Fernandez, Almudena, additional, Meinecke, Todd, additional, Meinert, Edward, additional, Milone, Michael C., additional, Mitchell, David A., additional, Muni, Niraj, additional, Nappi, Filomena, additional, Nathan, Neal H., additional, Ostuni, Emanuele, additional, Papakosta, Marianthi, additional, Paratore, Simona, additional, Pascali, Vincenzo Lorenzo, additional, Pernia, Cameron D., additional, Philipson, Benjamin, additional, Phillips, Fiona, additional, Phillips, James B., additional, Qureshi, Nasib, additional, Refolo, Pietro, additional, Ringo, Moira, additional, Robson, Matthew, additional, Ruff, Crystal, additional, Schmidt, Manuel, additional, Schroff, Matthias, additional, Scott, Michael J., additional, Sharpe, Michaela, additional, Sidman, Richard L., additional, Sinden, John D., additional, Smith, Devyn M., additional, Snyder, Evan Y., additional, Somara, Sita, additional, Spagnolo, Antonio Gioacchino, additional, Spinner, Daryl S., additional, Sridharan, Kanaka, additional, Sullivan, Michael, additional, Thompson, Keith, additional, Tobe, Brian T.D., additional, Vertès, Alain A., additional, West, Michael D., additional, Wilkins-Port, Cynthia, additional, Wittig, Burghardt, additional, Yang, Aidong, additional, Zhang, Jie, additional, and Zimmerman, Mark C., additional

Published
2020
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8. Long-term protection against SHIV89.6P replication in HIV-1 Tat vaccinated cynomolgus monkeys

Author

Maggiorella, Maria Teresa, Baroncelli, Silvia, Michelini, Zuleika, Fanales-Belasio, Emanuele, Moretti, Sonia, Sernicola, Leonardo, Cara, Andrea, Negri, Donatella R.M, Buttò, Stefano, Fiorelli, Valeria, Tripiciano, Antonella, Scoglio, Arianna, Caputo, Antonella, Borsetti, Alessandra, Ridolfi, Barbara, Bona, Roberta, Haaft, Peter ten, Macchia, Iole, Leone, Pasqualina, Pavone-Cossut, Maria Rosaria, Nappi, Filomena, Ciccozzi, Massimo, Heeney, Jonathan, Titti, Fausto, Cafaro, Aurelio, and Ensoli, Barbara

Published
2004
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12. HIV-1 Tat Promotes Integrin-Mediated HIV Transmission to Dendritic Cells by Binding Env Spikes and Competes Neutralization by Anti-HIV Antibodies

Author

Monini, Paolo, primary, Cafaro, Aurelio, additional, Srivastava, Indresh K., additional, Moretti, Sonia, additional, Sharma, Victoria A., additional, Andreini, Claudia, additional, Chiozzini, Chiara, additional, Ferrantelli, Flavia, additional, Cossut, Maria R. Pavone., additional, Tripiciano, Antonella, additional, Nappi, Filomena, additional, Longo, Olimpia, additional, Bellino, Stefania, additional, Picconi, Orietta, additional, Fanales-Belasio, Emanuele, additional, Borsetti, Alessandra, additional, Toschi, Elena, additional, Schiavoni, Ilaria, additional, Bacigalupo, Ilaria, additional, Kan, Elaine, additional, Sernicola, Leonardo, additional, Maggiorella, Maria T., additional, Montin, Katy, additional, Porcu, Marco, additional, Leone, Patrizia, additional, Leone, Pasqualina, additional, Collacchi, Barbara, additional, Palladino, Clelia, additional, Ridolfi, Barbara, additional, Falchi, Mario, additional, Macchia, Iole, additional, Ulmer, Jeffrey B., additional, Buttò, Stefano, additional, Sgadari, Cecilia, additional, Magnani, Mauro, additional, Federico, Maurizio P. M., additional, Titti, Fausto, additional, Banci, Lucia, additional, Dallocchio, Franco, additional, Rappuoli, Rino, additional, Ensoli, Fabrizio, additional, Barnett, Susan W., additional, Garaci, Enrico, additional, and Ensoli, Barbara, additional

Published
2012
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13. Immobilized HIV-1 Tat protein promotes gene transfer via a transactivation-independent mechanism which requires binding of Tat to viral particles

Author

Nappi, Filomena, primary, Chiozzini, Chiara, additional, Bordignon, Valentina, additional, Borsetti, Alessandra, additional, Bellino, Stefania, additional, Cippitelli, Marco, additional, Barillari, Giovanni, additional, Caputo, Antonella, additional, Tyagi, Mudit, additional, Giacca, Mauro, additional, and Ensoli, Barbara, additional

Published
2009
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14. HIV-1 Tat Addresses Dendritic Cells to Induce a Predominant Th1-Type Adaptive Immune Response That Appears Prevalent in the Asymptomatic Stage of Infection

Author

Fanales-Belasio, Emanuele, primary, Moretti, Sonia, additional, Fiorelli, Valeria, additional, Tripiciano, Antonella, additional, Pavone Cossut, Maria R., additional, Scoglio, Arianna, additional, Collacchi, Barbara, additional, Nappi, Filomena, additional, Macchia, Iole, additional, Bellino, Stefania, additional, Francavilla, Vittorio, additional, Caputo, Antonella, additional, Barillari, Giovanni, additional, Magnani, Mauro, additional, Laguardia, Maria Elena, additional, Cafaro, Aurelio, additional, Titti, Fausto, additional, Monini, Paolo, additional, Ensoli, Fabrizio, additional, and Ensoli, Barbara, additional

Published
2009
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17. Intracellular HIV-1 Tat protein represses constitutive LMP2 transcription increasing proteasome activity by interfering with the binding of IRF-1 to STAT1

Author

Remoli, Anna L., primary, Marsili, Giulia, additional, Perrotti, Edvige, additional, Gallerani, Eleonora, additional, Ilari, Ramona, additional, Nappi, Filomena, additional, Cafaro, Aurelio, additional, Ensoli, Barbara, additional, Gavioli, Riccardo, additional, and Battistini, Angela, additional

Published
2006
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19. Efficient mucosal delivery of the HIV-1 Tat protein using the synthetic lipopeptide MALP-2 as adjuvant

Author

Borsutzky, Stefan, primary, Fiorelli, Valeria, additional, Ebensen, Thomas, additional, Tripiciano, Antonella, additional, Rharbaoui, Faiza, additional, Scoglio, Arianna, additional, Link, Claudia, additional, Nappi, Filomena, additional, Morr, Michael, additional, Buttó, Stefano, additional, Cafaro, Aurelio, additional, Mühlradt, Peter F., additional, Ensoli, Barbara, additional, and Guzmán, Carlos A., additional

Published
2003
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20. HIV-1 Tat-Based Vaccines: From Basic Science to Clinical Trials

Author

Fanales-Belasio, Emanuele, primary, Cafaro, Aurelio, additional, Cara, Andrea, additional, Negri, Donatella R.M., additional, Fiorelli, Valeria, additional, Butto, Stefano, additional, Moretti, Sonia, additional, Maggiorella, Maria Teresa, additional, Baroncelli, Silvia, additional, Michelini, Zuleika, additional, Tripiciano, Antonella, additional, Sernicola, Leonardo, additional, Scoglio, Arianna, additional, Borsetti, Alessandra, additional, Ridolfi, Barbara, additional, Bona, Roberta, additional, ten Haaft, Peter, additional, Macchia, Iole, additional, Leone, Pasqualina, additional, Pavone-Cossut, Maria Rosaria, additional, Nappi, Filomena, additional, Vardas, Eftyhia, additional, Magnani, Mauro, additional, Laguardia, Elena, additional, Caputo, Antonella, additional, Titti, Fausto, additional, and Ensoli, Barbara, additional

Published
2002
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27. gag , vif , and nef Genes Contribute to the Homologous Viral Interference Induced by a Nonproducer Human Immunodeficiency Virus Type 1 (HIV-1) Variant: Identification of Novel HIV-1-Inhibiting Viral Protein Mutants

Author

D’Aloja, Paola, primary, Olivetta, Eleonora, additional, Bona, Roberta, additional, Nappi, Filomena, additional, Pedacchia, Daniela, additional, Pugliese, Katherina, additional, Ferrari, Giuliana, additional, Verani, Paola, additional, and Federico, Maurizio, additional

Published
1998
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28. The helical domain of GBP-1 mediates the inhibition of endothelial cell proliferation by inflammatory cytokines.

Author

Guenzi, Eric, Töpolt, Kristin, Cornali, Emmanuelle, Lubeseder-Martellato, Clara, Jörg, Anita, Matzen, Kathrin, Zietz, Christian, Kremmer, Elisabeth, Nappi, Filomena, Schwemmle, Martin, Hohenadl, Christine, Barillari, Giovanni, Tschachler, Erwin, Monini, Paolo, Ensoli, Barbara, and Stürzl, Michael

Subjects
CYTOKINES, CELL proliferation, CELL growth, NEOVASCULARIZATION, ANTINEOPLASTIC agents, LEUCOCYTES
Abstract

Inflammatory cytokines (IC) activate endothelial cell adhesiveness for monocytes and inhibit endothelial cell growth. Here we report the identification of the human guanylate binding protein-1 (GBP-1) as the key and specific mediator of the anti-proliferative effect of IC on endothelial cells. GBP-1 expression was induced by IC, downregulated by angiogenic growth factors, and inversely related to cell proliferation both in vitro in microvascular and macrovascular endothelial cells and in vivo in vessel endothelial cells of Kaposi's sarcoma. Experimental modulation of GBP-1 expression demonstrated that GBP-1 mediates selectively the anti-proliferative effect of IC, without affecting endothelial cell adhesiveness for monocytes. GBP-1 anti-proliferative activity did not affect ERK-1/2 activation, occurred in the absence of apoptosis, was found to be independent of the GTPase activity and isoprenylation of the molecule, but was specifically mediated by the C-terminal helical domain of the protein. These results define GBP-1 as an important tool for dissection of the complex activity of IC on endothelial cells, and detection and specific modulation of the IC-activated non-proliferating phenotype of endothelial cells in vascular diseases. [ABSTRACT FROM AUTHOR]

Published
2001
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30. gag, vif, and nefGenes Contribute to the Homologous Viral Interference Induced by a Nonproducer Human Immunodeficiency Virus Type 1 (HIV-1) Variant: Identification of Novel HIV-1-Inhibiting Viral Protein Mutants

Author

D’Aloja, Paola, Olivetta, Eleonora, Bona, Roberta, Nappi, Filomena, Pedacchia, Daniela, Pugliese, Katherina, Ferrari, Giuliana, Verani, Paola, and Federico, Maurizio

Abstract

ABSTRACTWe previously demonstrated that expression of the nonproducer F12-human immunodeficiency virus type 1 (HIV-1) variant induces a block in the replication of superinfecting HIV that does not depend on the down-regulation of CD4 HIV receptors. In order to individuate the gene(s) involved in F12-HIV-induced interference, vectors expressing each of the nine F12-HIV proteins were transfected in HIV-susceptible HeLa CD4 cells. Pools of cell clones stably producing each viral protein were infected with HIV-1, and virus release was measured in terms of reverse transcriptase activity in supernatants. We hereby demonstrate that HeLa CD4 cells expressing the F12-HIV gag, vif, ornefgene were resistant, to different degrees, to infection with T-cell-line-adapted HIV-1 strains. Conversely, expression of either the tat, rev, or vpuF12-HIV gene increased the rate of HIV release, and no apparent effects on HIV replication were observed in cells expressing either the F12-HIVvpr, pol, or envgene. No variation of CD4 exposure was detected in any of the uninfected HeLa CD4 pools. These data indicate that F12-HIV homologous viral interference is the consequence of the synergistic anti-HIV effects of Gag, Vif, and Nef proteins. Retrovirus vectors expressing F12-HIV vifornefallowed us to further establish that the expression of each mutated protein (i) inhibits the replication of clinical HIV-1 isolates as well, (ii) impairs the infectivity of the virus released by cells chronically infected with HIV-1, and (iii) limitedly to F12-HIV Vif protein, induces HIV resistance in both vif-permissive and vif-nonpermissive cells. The levels of action of F12-HIV vifand nefanti-HIV effects were also determined. We observed that HIV virions emerging from the first viral cycle on F12-HIV vif-expressing cells, although released in unaltered amounts, had a strongly reduced ability to initiate the retrotranscription process when they reinfected parental HeLa CD4 cells. Differently, we observed that expression of F12-HIV Nef protein affects the HIV life cycle at the level of viral assembling and/or release. For the first time, an inhibitory effect on the HIV life cycle in both acutely and chronically infected cells induced by mutated Vif and Nef HIV-1 proteins is described. These genes could thus be proposed as new useful reagents for anti-HIV gene therapy.

Published
1998
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31. Inhibition of trail gene expression by cyclopentenonic prostaglandin 15-deoxy-delta12,14-prostaglandin J2 in T lymphocytes.

Author

Fionda C, Nappi F, Piccoli M, Frati L, Santoni A, and Cippitelli M

Subjects
Base Sequence, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, Heat Shock Transcription Factors, Humans, Jurkat Cells, Lymphocyte Activation drug effects, Lymphocyte Activation genetics, PPAR gamma metabolism, Promoter Regions, Genetic drug effects, Prostaglandin D2 pharmacology, RNA, Messenger antagonists & inhibitors, RNA, Messenger metabolism, T-Lymphocytes immunology, TNF-Related Apoptosis-Inducing Ligand genetics, Transcription Factors genetics, Transcription Factors metabolism, Anti-Inflammatory Agents pharmacology, Gene Expression drug effects, Immunologic Factors pharmacology, Prostaglandin D2 analogs & derivatives, T-Lymphocytes drug effects, TNF-Related Apoptosis-Inducing Ligand antagonists & inhibitors
Abstract

15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) is a cyclopentenonic prostaglandin endowed with powerful anti-inflammatory activities, as shown in animal models of inflammatory/autoimmune diseases, where pharmacological administration of this prostanoid can ameliorate inflammation and local tissue damage via activation of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) and/or covalent modifications of cellular proteins. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF superfamily expressed in most of the cells, including those of immune system such as T lymphocytes, in which it is up-regulated upon antigen-specific stimulation. This cytokine plays an important role in regulating various physiological and immunopathological processes, such as immunosurveillance of tumors and tissue destruction associated with different inflammatory and autoimmune diseases. Here, we demonstrate that 15d-PGJ(2) inhibits trail mRNA and protein expression by down-regulating the activity of its promoter in human T lymphocytes. Our data indicate that both the chemically reactive cyclopentenone moiety of 15d-PGJ(2) and the activation of PPARgamma may be involved in this repressive mechanism. We identified nuclear factor kappaB (NF-kappaB) as a direct target of the prostanoid. 15d-PGJ(2) significantly decreases the expression and/or DNA binding of c-rel, RelA, and p50 transcription factors to the NF-kappaB1 site of trail promoter. Moreover, 15d-PGJ(2)-mediated activation of the transcription factor heat shock factor-1 may contribute to inhibit trail promoter activity in transfected Jurkat T cells. These results suggest that modulation of TRAIL gene expression by 15d-PGJ(2) in T cells may provide a novel pharmacological tool to modify the onset and the progression of specific autoimmune and inflammatory disorders.

Published
2007
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32. 15-deoxy-Delta12,14-prostaglandin J2 negatively regulates rankl gene expression in activated T lymphocytes: role of NF-kappaB and early growth response transcription factors.

Author

Fionda C, Nappi F, Piccoli M, Frati L, Santoni A, and Cippitelli M

Subjects
Animals, Base Sequence, Cells, Cultured, Down-Regulation, Early Growth Response Transcription Factors antagonists & inhibitors, Gene Expression drug effects, Gene Expression Regulation, Humans, Hybridomas drug effects, Lymphocyte Activation, Mice, Molecular Sequence Data, NF-kappa B antagonists & inhibitors, Promoter Regions, Genetic drug effects, Prostaglandin D2 pharmacology, RNA, Messenger antagonists & inhibitors, RNA, Messenger metabolism, T-Lymphocytes immunology, Early Growth Response Transcription Factors physiology, NF-kappa B physiology, Prostaglandin D2 analogs & derivatives, RANK Ligand genetics, T-Lymphocytes drug effects, Transcriptional Activation drug effects
Abstract

Receptor activator of NF-kappaB ligand (RANKL) and its receptor RANK are cell surface proteins abundantly expressed in bone and lymphoid tissues, whose interaction triggers different signaling pathways leading to activation and differentiation of osteoclasts, pivotal actors of the normal bone remodeling cycle. Moreover, RANKL may act as an immunomodulator, representing an important dendritic cell survival factor produced by activated T cells. A large body of research has shown that not only does the RANKL/RANK system regulate the physiology of bone development but also plays an important pathological role in bone destruction mediated by inflammatory disorders or bone metastatic tumors. 15-Deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. Although 15d-PGJ(2) has been studied as a natural ligand of the peroxisome proliferator-activated receptor-gamma nuclear receptor, relevant peroxisome proliferator-activated receptor-gamma-independent actions mediated by this prostanoid have been described. In this study, we describe the effect of 15d-PGJ(2) on the expression of the rankl gene in T lymphocytes. We show that 15d-PGJ(2) inhibits rankl mRNA expression, protein, and rankl promoter activity by mechanisms mediated by its chemically reactive cyclopentenone moiety. Our data also indicate that 15d-PGJ(2) represses rankl activation by interfering with the expression and/or activity of the transcription factors NF-kappaB, early growth response-2, and early growth response-3, whose altered balancing and transactivation may contribute for the repression of this gene. These results place rankl as a novel molecular target for the different immunoregulatory activities mediated by 15d-PGJ(2). The physiological and pharmacological implications of these observations are discussed.

Published
2007
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