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Giorgio Dieci

Researcher at University of Parma

Publications -  79
Citations -  3795

Giorgio Dieci is an academic researcher from University of Parma. The author has contributed to research in topics: RNA polymerase III & General transcription factor. The author has an hindex of 33, co-authored 77 publications receiving 3422 citations. Previous affiliations of Giorgio Dieci include University of Genoa & French Institute of Health and Medical Research.

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The expanding RNA polymerase III transcriptome.

TL;DR: The role of RNA polymerase (Pol) III in eukaryotic transcription is commonly thought of as being restricted to a small set of highly expressed, housekeeping non-protein-coding (nc)RNA genes, but recent studies have remarkably expanded the set of known Pol III-synthesized ncRNAs, suggesting that gene-specific Pol III regulation is more common than previously appreciated.
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Eukaryotic snoRNAs: a paradigm for gene expression flexibility.

TL;DR: A comprehensive account of snoRNA expressional freedom is provided by precisely estimating the frequency of each type of genomic organization in each genome by focusing on representative fungal, plant and animal genomes.
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17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease

TL;DR: It is demonstrated that 17A expression in neuroblastoma cells enhances the secretion of amyloid β peptide and the Aβ x-42/Α β x-40 peptide ratio and that its synthesis is induced in response to inflammatory stimuli, and correlated, for the first time, to neurodegeneration induced by abnormal GABA B function.
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Facilitated Recycling Pathway for RNA Polymerase III

TL;DR: Kinetic analysis shows that RNA polymerase recycling on preassembled tDNA.TFIIIB complexes is much faster than the initial transcription cycle, and template competition assays show that RNA pol III is committed to reinitiate on the same gene.
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An intronic ncRNA-dependent regulation of SORL1 expression affecting Aβ formation is upregulated in post-mortem Alzheimer's disease brain samples

TL;DR: 51A expression drives a splicing shift of SORL1 from the synthesis of the canonical long protein variant A to an alternatively spliced protein form, which is associated with impaired processing of amyloid precursor protein (APP), leading to increased Aβ formation.