G
Granata M
Researcher at University of Milan
Publications - 12
Citations - 715
Granata M is an academic researcher from University of Milan. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 9, co-authored 12 publications receiving 692 citations.
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Histone methyltransferase Dot1 and Rad9 inhibit single-stranded DNA accumulation at DSBs and uncapped telomeres This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution, and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation or the creation of derivative works without specific permission.
Federico Lazzaro,Vasileia Sapountzi,Granata M,Achille Pellicioli,Moreshwar B. Vaze,James E. Haber,Paolo Plevani,David Lydall,Marco Muzi-Falconi +8 more
TL;DR: It is suggested that both Rad9 and histone H3 methylation allow transmission of the damage signal to checkpoint kinases, and keep resection of damaged DNA under control influencing, both positively and negatively, checkpoint cascades and contributing to a tightly controlled response to DNA damage.
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Histone methyltransferase Dot1 and Rad9 inhibit single‐stranded DNA accumulation at DSBs and uncapped telomeres
Federico Lazzaro,Vasileia Sapountzi,Granata M,Achille Pellicioli,Moreshwar B. Vaze,James E. Haber,Paolo Plevani,David Lydall,Marco Muzi-Falconi +8 more
TL;DR: In this paper, Rad9 binding to histone H3-K79 methylated histone methylation has been shown to inhibit resection at DSBs and uncapped telomeres.
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Phosphorylation of the Budding Yeast 9-1-1 Complex Is Required for Dpb11 Function in the Full Activation of the UV-Induced DNA Damage Checkpoint
Fabio Puddu,Granata M,Lisa di Nola,Alessia Balestrini,Gabriele Piergiovanni,Federico Lazzaro,Michele Giannattasio,Paolo Plevani,Marco Muzi-Falconi +8 more
TL;DR: The data suggest that Dpb11 is held in proximity to damaged DNA through an interaction with the phosphorylated 9-1-1 complex, leading to Mec1-dependent phosphorylation of Rad9, and it is found that the replication factor Dpb 11 is the keystone of this second pathway.
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Checkpoint mechanisms at the intersection between DNA damage and repair
Federico Lazzaro,Michele Giannattasio,Fabio Puddu,Granata M,Achille Pellicioli,Paolo Plevani,Marco Muzi-Falconi +6 more
TL;DR: Interestingly, at least in some cases, if the damage level is low enough the cell can deal with the lesions and it does not need to activate the checkpoint response, and ifDamage level is high or if the lesions are not rapidly repairable, checkpoint mechanisms become important for cell survival and preservation of genome integrity.
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Dynamics of Rad9 chromatin binding and checkpoint function are mediated by its dimerization and are cell cycle-regulated by CDK1 activity.
Granata M,Federico Lazzaro,Daniele Novarina,Davide Panigada,Fabio Puddu,Carla M. Abreu,Ramesh Kumar,Muriel Grenon,Noel F. Lowndes,Paolo Plevani,Marco Muzi-Falconi +10 more
TL;DR: In G1 cells, GST or FKBP dimerization motifs can substitute to the BRCT domains for Rad9 chromatin binding and checkpoint function, and forced Rad9 diming in M phase fails to promote its recruitment onto DNA, although it supports Rad9 checkpoint function.