Zobrazeno 1 - 10
of 25
pro vyhledávání: '"Nadia Angeretti"'
Autor:
Nadia Angeretti, Ada De Luigi, Claudia Manzoni, Fabrizio Tagliavini, Alessio Colombo, Gianluigi Forloni, Roberto Chiesa, Luana Fioriti, Michela Morbin, Laura Colombo, Mario Salmona
Publikováno v:
The Journal of Neuroscience. 27:1576-1583
Amyloid fibrils in Gerstmann–Sträussler–Scheinker (GSS) disease are composed of a fragment of the prion protein (PrP), the N and C termini of which correspond to ragged residues 81–90 and 144–153. A synthetic peptide spanning the sequence 82
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::56406fdd1069d386ec65e0e209f44951
https://doi.org/10.1523/jneurosci.5145-06.2007
https://doi.org/10.1523/jneurosci.5145-06.2007
Publikováno v:
Scopus-Elsevier
Somatostatin (SRIF) exerts a modulatory function on neuronal transmission in the CNS. It has been proposed that a reduction of calcium currents is the major determinant of the inhibitory activity of this peptide on synaptic transmission. Because the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a6e6bf0b821120962740d8a969281b64
https://doi.org/10.1046/j.1471-4159.1997.68010319.x
https://doi.org/10.1046/j.1471-4159.1997.68010319.x
Autor:
Gianluigi Forloni, Lavinia Cantoni, M. Rizzardini, Mario Salmona, Nadia Angeretti, Roberto Chiesa, Elisa Lucca
Publikováno v:
Scopus-Elsevier
Heme oxygenase (HO), which catalyzes the degradation of heme, has two isozymes (HO-1 and HO-2). In brain the noninducible HO-2 isoform is predominant, whereas the inducible HO-1 is a marker of oxidative stress. Because brain oxidative stress might be
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::88c9867dd1b1e18259225f594b1d3cc8
https://doi.org/10.1046/j.1471-4159.1997.68020715.x
https://doi.org/10.1046/j.1471-4159.1997.68020715.x
Publikováno v:
Scopus-Elsevier
Beta-amyloid accumulates in cerebral deposits in Alzheimer's disease, so to test the correlation between the neurotoxic and fibrillogenic capacity of beta-amyloid, we synthesized a peptide homologous to fragment 25-35 of beta-amyloid (beta25-35) and
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c58e031b49cc86d3685dbac883959883
https://doi.org/10.1046/j.1471-4159.1997.69052048.x
https://doi.org/10.1046/j.1471-4159.1997.69052048.x
Autor:
Gianluigi Forloni, Elisa Lucca, Roberto Chiesa, Nadia Angeretti, Elettra Munna, Roberto Del Bo
Publikováno v:
Scopus-Elsevier
Cell viability and gene expression were studied in primary astroglial cells cultured in a nominally calcium-free medium. Ca2+ deprivation reduced progressively the astrocytes' viability, starting from 12 h; the restoration of a normal Ca2+ concentrat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7793ecc690399324765f1e1465445e0f
https://doi.org/10.1046/j.1471-4159.1998.70041474.x
https://doi.org/10.1046/j.1471-4159.1998.70041474.x
Autor:
Giacomina Rossi, Orso Bugiani, Fabrizio Tagliavini, Nadia Angeretti, Elisa Peressini, Enzio Ragg, Tazeen Awan, B. Canciani, Luca De Gioia, Lidia Giampaolo, Gianluigi Forloni, Mario Salmona, Laura Colombo, Laura Girola
Publikováno v:
Journal of Molecular Biology. 300:1309-1322
Prion diseases are characterized by the accumulation of altered forms of the prion protein (termed PrPSc) in the brain. Unlike the normal protein, PrPSc isoforms have a high content of β-sheet secondary structure, are protease-resistant, and form in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1c7246498a4a8b110634972bc621cc99
https://doi.org/10.1006/jmbi.2000.3840
https://doi.org/10.1006/jmbi.2000.3840
Autor:
Nadia Angeretti, Mario Salmona, Elisa Peressini, T. Rodriguez Martin, Gianluigi Forloni, P. Malesani, P. Della Torre
Publikováno v:
Annals of Neurology. 45:489-494
In transmissible spongiform encephalopathies (TSEs), an altered form of prion protein (PrP), PrPres, aggregates in amyloid fibrils and accumulates in the brain. Several point mutations of the PrP gene have been associated with the TSEs, so, to invest
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::c46cec0fd6ada149472bda5f6a1cc9f6
https://doi.org/10.1002/1531-8249(199904)45:4<489::aid-ana10>3.0.co
https://doi.org/10.1002/1531-8249(199904)45:4<489::aid-ana10>3.0.co
Publikováno v:
Cytokine. 9:759-762
The effect of a peptide homologous to the biologically active fragment of beta amyloid 25-35 (beta 25-35) was studied on interleukin 6 (IL-6) and tumour necrosis factor (TNF-alpha) secretion induced by lipopolysaccharide (LPS) in primary rat astrocyt
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4d22109db5f0505ae0f3d51a03f34fc7
https://doi.org/10.1006/cyto.1997.0232
https://doi.org/10.1006/cyto.1997.0232
Autor:
Fabrizio Tagliavini, Luisa Diomede, L. De Gioia, Marina Algeri, Gianluigi Forloni, Giorgio Giaccone, Nadia Angeretti, Mario Salmona, Orso Bugiani
Publikováno v:
Neurobiology of Disease, Vol 4, Iss 1, Pp 47-57 (1997)
Prion-related encephalopathies are characterized by astrogliosis and nerve cell degeneration and loss. These lesions might be the consequence of an interaction between the abnormal isoform of the cellular prion protein that accumulates in nervous tis
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1fd5f692bfc86c51dd4807a04dbc194a
http://www.sciencedirect.com/science/article/pii/S0969996197901339
http://www.sciencedirect.com/science/article/pii/S0969996197901339
Autor:
Fabrizio Tagliavini, Nadia Angeretti, Gianluigi Forloni, Mario Salmona, Roberto Chiesa, Elisa Lucca, Orso Bugiani
Publikováno v:
European Journal of Neuroscience. 8:589-597
Prion-related encephalopathies are characterized by the accumulation of an abnormal prion protein isoform (PrPSc) associated with neuronal degeneration and astrogliosis. The synthetic peptide homologous to PrP fragment 106-126 (PrP 106-126) induced i
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::621e731edb81042d1ea4bc099d151404
https://doi.org/10.1111/j.1460-9568.1996.tb01244.x
https://doi.org/10.1111/j.1460-9568.1996.tb01244.x