Topical Collection "Regulation by Non-Coding RNAs"

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A topical collection in International Journal of Molecular Sciences (ISSN 1422-0067). This collection belongs to the section "Biochemistry, Molecular Biology and Biophysics".

Editor

Collection Editor
Dr. Martin Pichler
Division of Clinical Oncology, Department of Medicine, Medical University of Graz, Auenbruggerplatz 15, Austria
Website: https://forschung.medunigraz.at/fodok/suchen.person_uebersicht?sprache_in=en&ansicht_in=&menue_id_in=101&id_in=2001296
E-Mail: martin.pichler@medunigraz.at
Interests: Non-coding RNAs; MicroRNAs; cancer; Inflammation; Metabolism; Gene expression; cancer stem cells; epithelial-mesenchymal transition

Topical Collection Information

Dear Colleagues,

Non-Coding RNAs are currently a hot research topic in many fields of biology, medicine, and chemistry. It is increasingly clear that non-coding RNAs are involved in fundamentally physiological and pathological processes. These processes touch on many important disciplines, from metabolism to cancer. Non-coding RNAs are regulative: they mainly influence biological processes by regulating other (protein-)coding gene expression. By doing this, the cellular properties of development and growth, stem cell regeneration, apoptosis, authophagy, etc., are strictly controlled by non-coding RNAs. This collection is dedicated to summarizing and highlighting the current research concerning the role of non-coding RNAs in regulating the aforementioned functions. The underlying mechanisms of action, the target molecules, the interactor pairs, and the pertinent cellular functions should all be presented. All relevant fields in medicine (with a special focus on metabolism, cancer, and inflammation) are of interest. The classes of non-coding RNAs should include microRNAs, other small non-coding RNAs, and long non-coding RNAs. Original research articles, review articles, and research letters are welcomed.

Dr. Martin Pichler
Collection Editor

Manuscript Submission Information

Manuscripts for the topical collection can be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on this website. The topical collection considers regular research articles, short communications and review articles. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs).

Keywords

  • Regulatory RNA
  • sRNA
  • ncRNA
  • lncRNA
  • miRNA
  • siRNA
  • piRNA
  • CRISPR RNA
  • regulatory small RNA fragments

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Published Papers (17 papers)

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2015  ( 8 papers )


2014  ( 9 papers )


2015
by , , , , ,  and
Int. J. Mol. Sci. 2015, 16(4), 6855-6867; doi:10.3390/ijms16046855 (registering DOI)
Received: 6 October 2014 / Revised: 10 November 2014 / Accepted: 13 November 2014 / Published: 26 March 2015
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by ,  and
Int. J. Mol. Sci. 2015, 16(3), 5467-5496; doi:10.3390/ijms16035467
Received: 12 December 2014 / Revised: 22 February 2015 / Accepted: 3 March 2015 / Published: 10 March 2015
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by ,  and
Int. J. Mol. Sci. 2015, 16(3), 4947-4972; doi:10.3390/ijms16034947
Received: 23 December 2014 / Revised: 17 February 2015 / Accepted: 17 February 2015 / Published: 4 March 2015
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Int. J. Mol. Sci. 2015, 16(2), 3251-3266; doi:10.3390/ijms16023251
Received: 17 November 2014 / Accepted: 22 January 2015 / Published: 3 February 2015
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by  and
Int. J. Mol. Sci. 2015, 16(1), 1395-1405; doi:10.3390/ijms16011395
Received: 16 December 2014 / Accepted: 30 December 2014 / Published: 8 January 2015
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by , , ,  and
Int. J. Mol. Sci. 2015, 16(1), 1448-1465; doi:10.3390/ijms16011448
Received: 1 December 2014 / Accepted: 30 December 2014 / Published: 8 January 2015
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by ,  and
Int. J. Mol. Sci. 2015, 16(1), 1466-1481; doi:10.3390/ijms16011466
Received: 31 October 2014 / Accepted: 5 January 2015 / Published: 8 January 2015
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by , , , , , , , , , ,  and
Int. J. Mol. Sci. 2015, 16(1), 1192-1208; doi:10.3390/ijms16011192
Received: 22 November 2014 / Accepted: 26 December 2014 / Published: 6 January 2015
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2014
by , ,  and
Int. J. Mol. Sci. 2014, 15(11), 21554-21586; doi:10.3390/ijms151121554
Received: 19 September 2014 / Revised: 7 November 2014 / Accepted: 8 November 2014 / Published: 24 November 2014
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by , , ,  and
Int. J. Mol. Sci. 2014, 15(11), 20434-20448; doi:10.3390/ijms151120434
Received: 17 September 2014 / Revised: 30 October 2014 / Accepted: 30 October 2014 / Published: 7 November 2014
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by ,  and
Int. J. Mol. Sci. 2014, 15(11), 20266-20289; doi:10.3390/ijms151120266
Received: 11 August 2014 / Revised: 22 October 2014 / Accepted: 27 October 2014 / Published: 6 November 2014
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by , , , , , , ,  and
Int. J. Mol. Sci. 2014, 15(11), 20134-20157; doi:10.3390/ijms151120134
Received: 29 May 2014 / Revised: 27 August 2014 / Accepted: 27 October 2014 / Published: 5 November 2014
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by , ,  and
Int. J. Mol. Sci. 2014, 15(9), 15891-15911; doi:10.3390/ijms150915891
Received: 11 July 2014 / Revised: 27 August 2014 / Accepted: 27 August 2014 / Published: 9 September 2014
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Int. J. Mol. Sci. 2014, 15(9), 15700-15733; doi:10.3390/ijms150915700
Received: 20 June 2014 / Revised: 5 August 2014 / Accepted: 13 August 2014 / Published: 4 September 2014
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by , ,  and
Int. J. Mol. Sci. 2014, 15(8), 14475-14491; doi:10.3390/ijms150814475
Received: 2 July 2014 / Revised: 7 August 2014 / Accepted: 12 August 2014 / Published: 20 August 2014
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by , , ,  and
Int. J. Mol. Sci. 2014, 15(8), 13993-14013; doi:10.3390/ijms150813993
Received: 30 June 2014 / Revised: 23 July 2014 / Accepted: 5 August 2014 / Published: 12 August 2014
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Int. J. Mol. Sci. 2014, 15(8), 13494-13513; doi:10.3390/ijms150813494
Received: 14 June 2014 / Revised: 14 July 2014 / Accepted: 28 July 2014 / Published: 4 August 2014
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Micro RNA-124a Regulates Lipolysis via Adipose Triglyceride Lipase and CGI-58
Authors:
Suman K. Das 1,, Paul W. Vesely 1,4,, Silvia Schauer 1, Anna Schwarz 1, Heimo Strohmaier 2, Thiery Claudel 3, Rudolf Zechner 4 and Gerald Hoefler 1,*
Affiliations:
1 Institute of Pathology, Medical University of Graz, Graz, Austria
2
Center for Medical Research, Medical University of Graz, Graz, Austria
3
Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
4
Institute of Molecular Biosciences, University of Graz, Graz, Austria
These authors contributed equally to this work.
*
Corresponding author: Gerald Hoefler, M.D., Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria; Tel.: +43-316-385-83654, e-mail: gerald.hoefler@medunigraz.at
Abstract
: Lipolysis is the biochemical pathway responsible for the catabolism of cellular triacylglycerol (TG). Lipolytic TG breakdown is a central metabolic process leading to the generation of free fatty acids (FA) and glycerol, thereby regulating lipid as well as energy homeostasis. The precise tuning of lipolysis is imperative to prevent lipotoxicity, obesity, diabetes and other related metabolic disorders.
Here, we present our finding that (miR)-124a is suppressing RNA and protein expression of the major TG hydrolase, adipose triglyceride lipase (ATGL/PNPLA2) and its co-activator comparative gene identification 58 (CGI-58/ABHD5). Ectopic expression of (miR)-124a in adipocytes leads to reduced lipolysis and increased cellular TG accumulation. This phenotype however, could be rescued by overexpressing Atgl without its 3’UTR, which harbors the identified (miR)-124a target site. In addition, we observed a strong negative correlation between (miR)-124a and ATGL expression in various murine tissues. Moreover, (miR)-124a regulated the expression of Atgl and Cgi-58 in murine white adipose tissue during fasting as well as the expression of Atgl in murine liver, during fasting and re-feeding. Together, these results suggest an instrumental role of (miR)-124a in the regulation of TG catabolism. We suggest that (miR)-124a may be involved in the regulation of several cellular and organismal metabolic parameters, including lipid storage and plasma fatty acid concentration.

Last update: 29 January 2015

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