Search Results - "De Maio, Antonia"
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Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model
Published in Neuron (Cambridge, Mass.) (19-10-2016)“…Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins. As growing evidence…”
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Pumilio1 Haploinsufficiency Leads to SCA1-like Neurodegeneration by Increasing Wild-Type Ataxin1 Levels
Published in Cell (12-03-2015)“…Spinocerebellar ataxia type 1 (SCA1) is a paradigmatic neurodegenerative proteinopathy, in which a mutant protein (in this case, ATAXIN1) accumulates in…”
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TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau
Published in eLife (25-10-2016)“…Several neurodegenerative diseases are driven by the toxic gain-of-function of specific proteins within the brain. Elevated levels of alpha-synuclein (α-Syn)…”
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Extensive cryptic splicing upon loss of RBM17 and TDP43 in neurodegeneration models
Published in Human molecular genetics (01-12-2016)“…Splicing regulation is an important step of post-transcriptional gene regulation. It is a highly dynamic process orchestrated by RNA-binding proteins (RBPs)…”
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RBM17 Interacts with U2SURP and CHERP to Regulate Expression and Splicing of RNA-Processing Proteins
Published in Cell reports (Cambridge) (16-10-2018)“…RNA splicing entails the coordinated interaction of more than 150 proteins in the spliceosome, one of the most complex of the cell’s molecular machines. We…”
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COUP-TFI promotes radial migration and proper morphology of callosal projection neurons by repressing Rnd2 expression
Published in Development (Cambridge) (01-11-2011)“…During corticogenesis, late-born callosal projection neurons (CPNs) acquire their laminar position through glia-guided radial migration and then undergo final…”
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Mecp2 Deletion from Cholinergic Neurons Selectively Impairs Recognition Memory and Disrupts Cholinergic Modulation of the Perirhinal Cortex
Published in eNeuro (01-11-2019)“…Rett Syndrome is a neurological disorder caused by mutations in the gene encoding methyl CpG binding protein 2 (MeCP2) and characterized by severe intellectual…”
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