Application of synthethic long non-coding RNAs to increase synthesis of Lysine (K)-specific demethylase 5C (KDM5C) in primary mouse neurons
| Autor: | Poeta L, Tuccillo M, Franco C, Canzoniero L, Zucchelli S, Gustincich S, Miano MG |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: | |
| Zdroj: | 19th International Workshop on Fragile X and other Neurodevelopmental Disorders, Sorrento, Naples, Italy, 18-21 September 2019 info:cnr-pdr/source/autori:Poeta L, Tuccillo M, Franco C, Canzoniero L, Zucchelli S, Gustincich S, Miano MG/congresso_nome:19th International Workshop on Fragile X and other Neurodevelopmental Disorders/congresso_luogo:Sorrento, Naples, Italy/congresso_data:18-21 September 2019/anno:2019/pagina_da:/pagina_a:/intervallo_pagine |
| Popis: | Impaired chromatin regulation has a critical role in the pathophysiology of several forms of Intellectual Disability (ID) with epilepsy in infancy and childhood. Lysine (K)-specific demethylase 5C (KDM5C) is an epigenetic regulator that removes di- and tri-methyl groups of lysine 4 on histone H3 (H3K4) from transcriptional targets and is essential for neuronal survival and dendritic growth. Mutations in KDM5C gene, located at Xp11.22, are an important cause of syndromic and non-syndromic XLID in males. Moreover, changes in KDM5C expression have been implicated in the pathology of ARX-related ID, Huntington's disease and drug addiction. Here we report on the application of an innovative long non-coding RNA-based technology named SINEUP for the role of Short Interspersed Nuclear Element B2 (SINEB2) to UP-regulate translation. The application of this innovative RNA-based therapy could open a new dimension to the field of nucleic acid based therapeutics for neurological "orphan" diseases with comorbid phenotypes. |
| Databáze: | OpenAIRE |
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