Tromp D, Dufour A, Lithfous S, Pebayle T, Despres O. Expression analysis of the long non-coding RNA antisense to Uchl1 (AS Uchl1) during dopaminergic cells’ differentiation in vitro and in neurochemical models of Parkinson’s disease. 2015 36:179–88.Ĭarrieri C, Forrest AR, Santoro C, Persichetti F, Carninci P, Zucchelli S, et al. Association between ubiquitin carboxy-terminal hydrolase-L1 S18Y variant and risk of Parkinson’s disease: the impact of ethnicity and onset age. Liu Y, Chen YY, Liu H, Yao CJ, Zhu XX, Chen DJ, et al. Expression of non-protein-coding antisense RNAs in genomic regions related to autism spectrum disorders. A noncoding RNA antisense to moesin at 5p14.1 in autism. Kerin T, Ramanathan A, Rivas K, Grepo N, Coetzee GA, Campbell DB. An architectural role for a nuclear noncoding RNA: NEAT1 RNA is essential for the structure of paraspeckles. 2017 18:627–40.Ĭlemson CM, Hutchinson JN, Sara SA, Ensminger AW, Fox AH, Chess A, et al. Long noncoding RNAs: molecular modalities to organismal functions. Architectural and functional commonalities between enhancers and promoters. Enhancer RNA facilitates NELF release from immediate early genes. Schaukowitch K, Joo JY, Liu X, Watts JK, Martinez C, Kim TK. Stimulus-specific combinatorial functionality of neuronal c-fos enhancers. Joo JY, Schaukowitch K, Farbiak L, Kilaru G, Kim TK. Enhancer RNAs: a class of long noncoding RNAs synthesized at enhancers. Towards a complete map of the human long non-coding RNA transcriptome. Uszczynska-Ratajczak B, Lagarde J, Frankish A, Guigo R, Johnson R. NONCODE 2016: an informative and valuable data source of long non-coding RNAs. Zhao Y, Li H, Fang S, Kang Y, Wu W, Hao Y, et al. Genome-wide analysis reveals distinct patterns of epigenetic features in long non-coding RNA loci. Sati S, Ghosh S, Jain V, Scaria V, Sengupta S. Deregulated expression of mammalian lncRNA through loss of SPT6 induces R-loop formation, replication stress, and cellular senescence. Nojima T, Tellier M, Foxwell J, Ribeiro de Almeida C, Tan-Wong SM, Dhir S, et al.
Parental imprinting of the mouse H19 gene. A gene from the region of the human X inactivation centre is expressed exclusively from the inactive X chromosome. 2012 81:145–66.īrown CJ, Ballabio A, Rupert JL, Lafreniere RG, Grompe M, Tonlorenzi R, et al. Genome regulation by long noncoding RNAs. Novel classes of non-coding RNAs and cancer. Sana J, Faltejskova P, Svoboda M, Slaby O. Functional classification and experimental dissection of long noncoding RNAs. Landscape of transcription in human cells. 2013 110:5294–300.ĭjebali S, Davis CA, Merkel A, Dobin A, Lassmann T, Mortazavi A, et al. We also discuss potential targets of lncRNAs and their promise as novel therapeutics and biomarkers in brain disorders.ĭoolittle WF. In this review, we discuss the recent progress in the study of lncRNAs, and addresses the pathogenesis of brain disorders that involve lncRNAs and describes the associations of lncRNAs with neurodegenerative disorders such as Alzheimer disease (AD), Parkinson disease (PD), and neurodevelopmental disorders.
High-throughput screening-based sequencing has been instrumental in identification of lncRNAs that demand new approaches to understanding the progression of brain disorders. Accumulating evidence suggests the potential of lncRNAs as diagnostic or prognostic biomarkers and therapeutic targets. Recently, long noncoding RNAs (lncRNAs) which are longer than 200 nucleotides in length have been suggested as key factors in various brain disorders. Through the cooperation of gene transcripts in biological processes, the study of noncoding RNAs can lead to insights into the cause and treatment of brain disorders. According to current paradigms, various risk factors, such as genetic mutations, oxidative stress, neural network dysfunction, and abnormal protein degradation, contribute to the progression of brain disorders.
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