Next Issue
Previous Issue

Table of Contents

Non-Coding RNA, Volume 2, Issue 4 (December 2016)

  • Issues are regarded as officially published after their release is announced to the table of contents alert mailing list.
  • You may sign up for e-mail alerts to receive table of contents of newly released issues.
  • PDF is the official format for papers published in both, html and pdf forms. To view the papers in pdf format, click on the "PDF Full-text" link, and use the free Adobe Readerexternal link to open them.
View options order results:
result details:
Displaying articles 1-5
Export citation of selected articles as:

Research

Jump to: Other

Open AccessArticle Regulation of the U3-, U8-, and U13snoRNA Expression by the DEAD Box Proteins Ddx5/Ddx17 with Consequences for Cell Proliferation and Survival
Non-Coding RNA 2016, 2(4), 11; doi:10.3390/ncrna2040011
Received: 6 June 2016 / Revised: 22 July 2016 / Accepted: 9 August 2016 / Published: 30 September 2016
PDF Full-text (2734 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Small nucleolar RNAs (snoRNAs) in cooperation with their associated proteins (snoRNPs) contribute to the maturation of ribosomal RNA, transfer RNA, and other transcripts. Most snoRNPs mediate chemical base modifications of their RNA substrates, and a few others, like those formed by the C/D
[...] Read more.
Small nucleolar RNAs (snoRNAs) in cooperation with their associated proteins (snoRNPs) contribute to the maturation of ribosomal RNA, transfer RNA, and other transcripts. Most snoRNPs mediate chemical base modifications of their RNA substrates, and a few others, like those formed by the C/D snoRNAs U3, U8, and U13, are needed for the structural organization and maturation of primary transcripts. The U3-, U8-, and U13snoRNAs are encoded by autonomous genes, and our knowledge about their expression regulation is limited. In this study, a significant increase in the concentrations of U3-, U8-, and U13snoRNA after a knockdown of DEAD box proteins Ddx5/Ddx17 in HeLa cells is observed. These alterations are shown to be caused by transcriptional suppression mediated by Ddx5/Ddx17 via histone deacetylase 1 in a promoter-dependent way. The biological function of this expression control may be related to the role of Ddx5/Ddx17 in cell proliferation. The U3snoRNA is shown here to be essential for the proliferation and viability of human cells. Moreover, it was found that U3snoRNA interacts with Argonaute 2 in the RNA-induced silencing complexes (RISC), pointing to a microRNA-like function. For this reason, the 3′ untranslated region of the A-kinase anchor protein 9 (AKAP9)-mRNA could be identified as a potential target. Full article
Figures

Figure 1

Open AccessArticle TWEAK Negatively Regulates Human Dicer
Non-Coding RNA 2016, 2(4), 12; doi:10.3390/ncrna2040012
Received: 7 September 2016 / Revised: 7 October 2016 / Accepted: 14 October 2016 / Published: 25 October 2016
PDF Full-text (2923 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The ribonuclease Dicer plays a central role in the microRNA pathway by processing microRNA precursors (pre-microRNAs) into microRNAs, a class of 19- to 24-nucleotide non-coding RNAs that regulate expression of ≈60% of the genes in humans. To gain further insights into the function
[...] Read more.
The ribonuclease Dicer plays a central role in the microRNA pathway by processing microRNA precursors (pre-microRNAs) into microRNAs, a class of 19- to 24-nucleotide non-coding RNAs that regulate expression of ≈60% of the genes in humans. To gain further insights into the function and regulation of Dicer in human cells, we performed a yeast two-hybrid (Y2HB) screen using human Dicer double-stranded RNA-binding domain (dsRBD) as bait. This approach identified tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) as a Dicer-interacting protein candidate. Confocal immunofluorescence microscopy revealed the colocalization of Dicer and TWEAK proteins at the perinuclear region of HeLa cells. The Dicer-TWEAK protein interaction was confirmed by coimmunoprecipitation and found not likely to be mediated by RNA. TWEAK dose-dependently reduced pre-microRNA conversion into mature microRNA in Dicer activity assays using extracts of transfected human HEK 293 cells. TWEAK expression also impaired microRNA-guided RNA silencing of a reporter gene induced by a pre-microRNA. These findings suggest a role for TWEAK—a pro-inflammatory cytokine—in regulating Dicer function and microRNA biogenesis, and its possible involvement in regulating gene expression during inflammatory processes and diseases. Full article
Figures

Figure 1

Open AccessCommunication High Percentage of Isomeric Human MicroRNA and Their Analytical Challenges
Non-Coding RNA 2016, 2(4), 13; doi:10.3390/ncrna2040013
Received: 16 September 2016 / Revised: 25 October 2016 / Accepted: 23 November 2016 / Published: 2 December 2016
Cited by 1 | PDF Full-text (13600 KB) | HTML Full-text | XML Full-text
Abstract
MicroRNA (miR) are short non-coding RNAs known to post-transcriptionally regulate gene expression, and have been reported as biomarkers for various diseases. miR have also been served as potential drug targets. The identity, functions and detection of a specific miR are determined by its
[...] Read more.
MicroRNA (miR) are short non-coding RNAs known to post-transcriptionally regulate gene expression, and have been reported as biomarkers for various diseases. miR have also been served as potential drug targets. The identity, functions and detection of a specific miR are determined by its RNA sequence, whose composition is made up of only 4 canonical ribonucleotides. Hence, among over two thousand human miR, their nucleotide compositions are expected to be similar but the extent of similarity has not been reported. In this study, the sequences of mature human miR were downloaded from miRBase, and collated using different tools to determine and compare their nucleotide compositions and sequences. 55% of all human miR were found to be structural isomers. The structural isomers of miR (SimiR) are defined as having the same size and identical nucleotide composition. A number of SimiR were also found to have high sequence similarities. To investigate the extent of SimiR in biological samples, three disease models were chosen, and disease-associated miR were identified from miR2Disease. Among the disease models, as high as 73% of miR were found to be SimiR. This report provides the missing information about human miR and highlights the challenges on the detection of SimiR. Full article
Figures

Figure 1

Open AccessCommunication Current perspectives in Set7 mediated stem cell differentiation
Non-Coding RNA 2016, 2(4), 14; doi:10.3390/ncrna2040014
Received: 26 October 2016 / Revised: 18 November 2016 / Accepted: 23 November 2016 / Published: 4 December 2016
PDF Full-text (624 KB) | HTML Full-text | XML Full-text
Abstract
Set7 is a key regulatory enzyme involved in the methylation of lysine residues of histone and non-histone proteins. This lysine methyltransferase is induced during stem cell differentiation and regulates lineage specific gene transcription and cell fate. In this article we discuss recent experimental
[...] Read more.
Set7 is a key regulatory enzyme involved in the methylation of lysine residues of histone and non-histone proteins. This lysine methyltransferase is induced during stem cell differentiation and regulates lineage specific gene transcription and cell fate. In this article we discuss recent experimental evidence identifying regulatory targets under the control of Set7 as well as emerging evidence of regulation in stem cell differentiation. Furthermore, we discuss the function of non-coding RNAs regulated by Set7 implicated in cell plasticity. Full article
(This article belongs to the Special Issue The Biology of Non-Coding RNAs and Metabolic Diseases)
Figures

Figure 1

Other

Jump to: Research

Open AccessErratum Erratum: The Non-Coding RNA Journal Club: Highlights on Recent Papers—4. Non-Coding RNA 2016, 2, 9
Non-Coding RNA 2016, 2(4), 10; doi:10.3390/ncrna2040010
Received: 28 September 2016 / Accepted: 28 September 2016 / Published: 30 September 2016
PDF Full-text (154 KB) | HTML Full-text | XML Full-text
Abstract Please note that in the published editorial [1], affiliations 1, and 8 contained errors.[...] Full article

Journal Contact

MDPI AG
ncRNA Editorial Office
St. Alban-Anlage 66, 4052 Basel, Switzerland
E-Mail: 
Tel. +41 61 683 77 34
Fax: +41 61 302 89 18
Editorial Board
Contact Details Submit to ncRNA Edit a special issue Review for ncRNA
logo
loading...
Back to Top