Could IncRNAs contribute to β-cell identity and its loss in Type 2 diabetes?

被引：12

作者：

Pullen, Timothy J. ^{[1
]}

Rutter, Guy A. ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Dept Med, Sect Cell Biol, London SW7 2AZ, England

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2013年 / 41卷

基金：

英国惠康基金;

关键词：

beta-cell; chromatin; epigenetics; islet; long non-coding RNA (IncRNA); Type; 2; diabetes; LONG NONCODING RNA; DUTCH HUNGER WINTER; INSULIN-SECRETION; LACTATE-DEHYDROGENASE; PANCREATIC-ISLET; EXPRESSION; GLUCOSE; TRANSCRIPTION; GENE; DIFFERENTIATION;

D O I：

10.1042/BST20120355

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The progression of Type 2 diabetes is accompanied by diminishing islet beta-cell mass and function. It has been proposed that beta-cells are lost not only through apoptosis, but also by dedifferentiating into progenitor-like cells. There is therefore much interest in the mechanisms which define and maintain beta-cell identity. The advent of genome-wide analyses of chromatin modifications has highlighted the role of epigenetic factors in determining cell identity. There is also evidence from both human populations and animal models for an epigenetic component in susceptibility to Type 2 diabetes. The mechanisms responsible for defining the epigenetic landscape in individual cell types are poorly understood, but there is growing evidence of a role for IncRNAs (long non-coding RNAs) in this process. In the present paper, we discuss some of the mechanisms through which IncRNAs may contribute to beta-cell identity and Type 2 diabetes risk.

引用

页码：797 / 801

页数：5

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