12 Citazioni (Scopus)

Abstract

Background: Hutchinson-Gilford progeria syndrome is a rare dominant human disease of genetic origin. Theaverage life expectancy is about 20 years, patients’ life quality is still very poor and no efficient therapy has yet beendeveloped. It is caused by mutation of the LMNA gene, which results in accumulation in the nuclear membrane ofa particular splicing form of Lamin-A called progerin. The mechanism by which progerin perturbs cellularhomeostasis and leads to the symptoms is still under debate.Micro-RNAs are able to negatively regulate transcription by coupling with the 3’ UnTranslated Region of messengerRNAs. Several Micro-RNAs recognize the same 3’ UnTranslated Region and each Micro-RNA can recognize multiple3’ UnTranslated Regions of different messenger RNAs. When different messenger RNAs are co-regulated via a similarpanel of micro-RNAs, these messengers are called Competing Endogenous RNAs, or ceRNAs.The 3’ UnTranslated Region of the longest LMNA transcript was analysed looking for its ceRNAs. The aim of thisstudy was to search for candidate genes and gene ontology functions possibly influenced by LMNA mutations thatmay exert a role in progeria development.Results: 11 miRNAs were isolated as potential LMNA regulators. By computational analysis, the miRNAs pointed to17 putative LMNA ceRNAs. Gene ontology analysis of isolated ceRNAs showed an enrichment in RNA interferenceand control of cell cycle functions.Conclusion: This study isolated novel genes and functions potentially involved in LMNA network of regulation thatcould be involved in laminopathies such as the Hutchinson-Gilford progeria syndrome
Lingua originaleEnglish
pagine (da-a)1-22
Numero di pagine0
RivistaJournal of Clinical Bioinformatics
Volume3
Stato di pubblicazionePublished - 2013

All Science Journal Classification (ASJC) codes

  • Health Informatics

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