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Role of non-coding RNAs in pancreatic beta-cell development and physiology.

Eliasson, Lena LU orcid and Esguerra, Jonathan LU orcid (2014) In Acta Physiologica 211(2). p.273-284
Abstract
The progression of diabetes is accompanied by increasing demand to the beta-cells to produce and secrete more insulin, requiring complex beta-cell adaptations. Functionally-active and ubiquitous non-coding RNAs (ncRNAs) have the capacity to take part in such adaptations as they have been shown to be key regulatory molecules in various biological processes. In the pancreatic islets, the function of ncRNAs and their contribution to disease development is beginning to be understood. Here, we review the different classes of ncRNAs, such as long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), and their potential contribution to insulin secretion. A special focus will be on miRNAs and their regulatory function in beta-cell physiology and... (More)
The progression of diabetes is accompanied by increasing demand to the beta-cells to produce and secrete more insulin, requiring complex beta-cell adaptations. Functionally-active and ubiquitous non-coding RNAs (ncRNAs) have the capacity to take part in such adaptations as they have been shown to be key regulatory molecules in various biological processes. In the pancreatic islets, the function of ncRNAs and their contribution to disease development is beginning to be understood. Here, we review the different classes of ncRNAs, such as long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), and their potential contribution to insulin secretion. A special focus will be on miRNAs and their regulatory function in beta-cell physiology and insulin exocytosis. As important players in gene regulation, ncRNAs have huge potential in opening innovative therapeutic avenues against diabetes and associated complications. This article is protected by copyright. All rights reserved. (Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Acta Physiologica
volume
211
issue
2
pages
273 - 284
publisher
Wiley-Blackwell
external identifiers
  • pmid:24666639
  • wos:000335911600007
  • scopus:84900811419
  • pmid:24666639
ISSN
1748-1716
DOI
10.1111/apha.12285
language
English
LU publication?
yes
id
d710dde6-e14a-4716-b39c-82eec02d5429 (old id 4379725)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24666639?dopt=Abstract
date added to LUP
2016-04-01 10:15:26
date last changed
2022-04-20 00:20:03
@article{d710dde6-e14a-4716-b39c-82eec02d5429,
  abstract     = {{The progression of diabetes is accompanied by increasing demand to the beta-cells to produce and secrete more insulin, requiring complex beta-cell adaptations. Functionally-active and ubiquitous non-coding RNAs (ncRNAs) have the capacity to take part in such adaptations as they have been shown to be key regulatory molecules in various biological processes. In the pancreatic islets, the function of ncRNAs and their contribution to disease development is beginning to be understood. Here, we review the different classes of ncRNAs, such as long noncoding RNAs (lncRNAs) and microRNAs (miRNAs), and their potential contribution to insulin secretion. A special focus will be on miRNAs and their regulatory function in beta-cell physiology and insulin exocytosis. As important players in gene regulation, ncRNAs have huge potential in opening innovative therapeutic avenues against diabetes and associated complications. This article is protected by copyright. All rights reserved.}},
  author       = {{Eliasson, Lena and Esguerra, Jonathan}},
  issn         = {{1748-1716}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{273--284}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Acta Physiologica}},
  title        = {{Role of non-coding RNAs in pancreatic beta-cell development and physiology.}},
  url          = {{http://dx.doi.org/10.1111/apha.12285}},
  doi          = {{10.1111/apha.12285}},
  volume       = {{211}},
  year         = {{2014}},
}