Zobrazeno 1 - 10 of 15 pro vyhledávání: '"Fabrizia Marullo"'
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Akademický článek
SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome
Autor: Endre Sebestyén, Fabrizia Marullo, Federica Lucini, Cristiano Petrini, Andrea Bianchi, Sara Valsoni, Ilaria Olivieri, Laura Antonelli, Francesco Gregoretti, Gennaro Oliva, Francesco Ferrari, Chiara Lanzuolo
Publikováno v: Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
Hutchinson-Gilford progeria syndrome is a genetic disease where an aberrant form of Lamin A disrupts chromatin by interfering with lamina associated domains. Here, the authors present the SAMMY-seq, a method for genome-wide characterization of hetero
Externí odkaz: https://doaj.org/article/2551c3f1e7794b139aa2db7812391766
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2
Akademický článek
Phosphodiesterase 10 inhibition reduces striatal excitotoxicity in the quinolinic acid model of Huntington's disease
Autor: Carmela Giampà, Stefano Patassini, Antonella Borreca, Daunia Laurenti, Fabrizia Marullo, Giorgio Bernardi, Frank S. Menniti, Francesca R. Fusco
Publikováno v: Neurobiology of Disease, Vol 34, Iss 3, Pp 450-456 (2009)
Decreased activity of cAMP responsive element-binding protein (CREB) is thought to contribute to the death of striatal medium spiny neurons in Huntington's disease (HD). Therefore, therapies that increase levels of activated CREB, may be effective in
Externí odkaz: https://doaj.org/article/4814046872504ea1bbcb03c445236dc1
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4
SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome
Autor: Cristiano Petrini, Chiara Lanzuolo, Gennaro Oliva, Endre Sebestyén, Federica Lucini, Sara Valsoni, Francesco Ferrari, Louis Antonelli, Andrea Bianchi, Francesco Gregoretti, Fabrizia Marullo, Ilaria Olivieri
Publikováno v: Nature Communications
Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
Nature communications 11 (2020): 6274. doi:10.1038/s41467-020-20048-9
info:cnr-pdr/source/autori:Sebestyen E, Marullo F, Lucini F, Petrini C, Bianchi A, Valsoni S, Olivieri I, Antonelli L, Gregoretti F, Oliva G, Ferrari F, Lanzuolo C./titolo:SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome/doi:10.1038%2Fs41467-020-20048-9/rivista:Nature communications/anno:2020/pagina_da:6274/pagina_a:/intervallo_pagine:6274/volume:11
Hutchinson-Gilford progeria syndrome is a genetic disease caused by an aberrant form of Lamin A resulting in chromatin structure disruption, in particular by interfering with lamina associated domains. Early molecular alterations involved in chromati
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ca8574e26d8af1183ec0f4c4f1005097
https://pubmed.ncbi.nlm.nih.gov/33293552
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5
Early Polycomb-target deregulations in Hutchinson-Gilford Progeria Syndrome revealed by heterochromatin analysis
Autor: Cristiano Petrini, Fabrizia Marullo, Sara Valsoni, Federica Lucini, Louis Antonelli, Francesco Ferrari, Ilaria Olivieri, Andrea Bianchi, Francesco Gregoretti, Chiara Lanzuolo, Endre Sebestyén, Gennaro Oliva
Hutchinson-Gilford progeria syndrome (HGPS) is characterized by the progressive accumulation of progerin, an aberrant form of Lamin A. This leads to chromatin structure disruption, in particular by interfering with Lamina Associated Domains. Although
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9b7ad8f27a9ed632d285583806b91a73
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6
Nucleoplasmic Lamin A/C and Polycomb group of proteins: An evolutionarily conserved interplay
Autor: Francesco Gregoretti, Gennaro Oliva, Elisa Cesarini, Chiara Lanzuolo, Louis Antonelli, Fabrizia Marullo
Publikováno v: Nucleus
Nucleus (Austin, Tex. : Print) 7 (2016): 103–111. doi:10.1080/19491034.2016.1157675
info:cnr-pdr/source/autori:Marullo F.; Cesarini E.; Antonelli L.; Gregoretti F.; Oliva G.; Lanzuolo C./titolo:Nucleoplasmic Lamin A%2FC and Polycomb group of proteins: An evolutionarily conserved interplay/doi:10.1080%2F19491034.2016.1157675/rivista:Nucleus (Austin, Tex. : Print)/anno:2016/pagina_da:103/pagina_a:111/intervallo_pagine:103–111/volume:7
Nuclear lamins are the main components of the nuclear lamina at the nuclear periphery, providing mechanical support to the nucleus. However, recent findings suggest that lamins also reside in the nuclear interior, as a distinct and dynamic pool with
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::08ebe3e27518ebd55332238f1244f053
http://europepmc.org/articles/PMC4916880
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7
Early chromatin conformational changes in Hutchinson-Gilford progeria syndrome revealed by heterochromatin analysis
Autor: Endre Sebestyén, Fabrizia Marullo, Federica Lucini, Sara Valsoni, Laura Antonelli, Francesco Gregoretti, Gennaro Oliva, Francesco Ferrari, Chiara Lanzuolo
Publikováno v: The Progeria Research Foundation 9th International Scientific Workshop, 20-22/09/2018
info:cnr-pdr/source/autori:Endre Sebestyén, Fabrizia Marullo, Federica Lucini,Sara Valsoni, Laura Antonelli, Francesco Gregoretti, Gennaro Oliva, Francesco Ferrari and Chiara Lanzuolo/congresso_nome:The Progeria Research Foundation 9th International Scientific Workshop/congresso_luogo:/congresso_data:20-22%2F09%2F2018/anno:2018/pagina_da:/pagina_a:/intervallo_pagine
Principles of Chromosome Structure and Function, EMBL Heidelberg, Germany, 5-8/09/2018
info:cnr-pdr/source/autori:Endre Sebestyén, Fabrizia Marullo, Federica Lucini,Sara Valsoni, Laura Antonelli, Francesco Gregoretti, Gennaro Oliva, Francesco Ferrari and Chiara Lanzuolo/congresso_nome:Principles of Chromosome Structure and Function/congresso_luogo:EMBL Heidelberg, Germany/congresso_data:5-8%2F09%2F2018/anno:2018/pagina_da:/pagina_a:/intervallo_pagine
Hutchinson-Gilford Progeria Syndrome (HGPS) is characterized by the progressive accumulation of progerin, an aberrant form of Lamin A, leading to chromatin structure disruption, in particular by interfering with Lamina Associated Domains. Although se
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::66e2296eaaf21917a3c8edcfbfbe33aa
http://www.cnr.it/prodotto/i/395826
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8
Lamin A/C sustains PcG protein architecture, maintaining transcriptional repression at target genes
Autor: Louis Antonelli, Elisa Cesarini, Alice Cortesi, Gennaro Oliva, Chiara Mozzetta, Beatrice Bodega, Simona Di Pelino, Francesco Gregoretti, Chiara Lanzuolo, Fabrizia Marullo, Stefano Squarzoni, Marta Columbaro, Alessio Zippo, Daniela Palacios, Annagiusi Gargiulo
Publikováno v: The Journal of Cell Biology
The Journal of cell biology 211 (2015): 533–551. doi:10.1083/jcb.201504035
info:cnr-pdr/source/autori:Elisa Cesarini, Chiara Mozzetta, Fabrizia Marullo, Francesco Gregoretti, Annagiusi Gargiulo, Marta Columbaro, Alice Cortesi, Laura Antonelli, Simona Di Pelino, Stefano Squarzoni, Daniela Palacios, Alessio Zippo, Beatrice Bodega, Gennaro Oliva and Chiara Lanzuolo/titolo:Lamin A%2FC sustains PcG proteins architecture maintaining transcriptional repression at target genes/doi:10.1083%2Fjcb.201504035/rivista:The Journal of cell biology/anno:2015/pagina_da:533/pagina_a:551/intervallo_pagine:533–551/volume:211
Reduction of lamin A/C, which is evolutionarily required for the modulation of Polycomb group (PcG) protein–dependent transcriptional repression by sustaining PcG protein nuclear architecture, leads to PcG protein diffusion and to muscle differenti
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a09c9bc9504df4201fbf35b0ab6f70a6
http://europepmc.org/articles/PMC4639869
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9
Determination of Polycomb Group of Protein Compartmentalization Through Chromatin Fractionation Procedure
Autor: Federica, Marasca, Fabrizia, Marullo, Chiara, Lanzuolo
Publikováno v: Methods in molecular biology (Clifton, N.J.). 1480
Epigenetic mechanisms modulate and maintain the transcriptional state of the genome acting at various levels on chromatin. Emerging findings suggest that the position in the nuclear space and the cross talk between components of the nuclear architect
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::0efa67dd3cf7f8b6b52c8faf73fbf950
https://pubmed.ncbi.nlm.nih.gov/27659984
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10
An evolutionarily acquired genotoxic response discriminates MyoD from Myf5, and differentially regulates hypaxial and epaxial myogenesis
Autor: Anna Innocenzi, Pier Lorenzo Puri, Giulio Cossu, Coralie Poizat, Fabrizia Marullo, Marta Simonatto, Lucia Latella, Graziella Messina, Jean Y. J. Wang, Chih-Wen Shu, Libera Berghella
Publikováno v: EMBO reports. 12:164-171
Despite having distinct expression patterns and phenotypes in mutant mice, the myogenic regulatory factors Myf5 and MyoD have been considered to be functionally equivalent. Here, we report that these factors have a different response to DNA damage, d
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1fdfcf3509b5bf04d21a7caaf52fb6f0
https://doi.org/10.1038/embor.2010.195
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