Literature DB >> 31271897

Maternally expressed gene 3 in metabolic programming.

Samuel Hamilton1, Rafael de Cabo1, Michel Bernier2.   

Abstract

Maternally Expressed Gene 3 (MEG3) is a long noncoding RNA (lncRNA) that coordinates a diverse array of cellular processes requiring epigenetic regulation of genes and interactions with key signaling proteins and by acting as a competitive endogenous (ce)RNA. Epigenetic modifications driven by in utero nutrition affect MEG3 expression and its role in the development of multiple metabolic disorders. This review examines how epigenetic modification of MEG3 expression can confer adaptedness to different metabolic environments. To this end, we discuss how nutritional status that leads to an increase of MEG3 expression can protect against cancer and metabolic dysfunctions, while interventions that promote MEG3 downregulation minimize the pleiotropic costs associated with its expression. Lastly, we identify research directions that would further shed light on the role of MEG3 in metabolic regulation and in functional imprinted gene networks. This article is part of a Special Issue entitled: ncRNA in control of gene expression edited by Kotb Abdelmohsen. Published by Elsevier B.V.

Entities:  

Keywords:  Epigenetic imprinting; MEG3; Metabolic programming; miRNA sponge

Mesh:

Substances:

Year:  2019        PMID: 31271897      PMCID: PMC6938580          DOI: 10.1016/j.bbagrm.2019.06.007

Source DB:  PubMed          Journal:  Biochim Biophys Acta Gene Regul Mech        ISSN: 1874-9399            Impact factor:   4.490


  138 in total

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3.  CREB-upregulated lncRNA MEG3 promotes hepatic gluconeogenesis by regulating miR-302a-3p-CRTC2 axis.

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4.  Apal polymorphism in insulin-like growth factor II (IGF2) gene and weight in middle-aged males.

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Review 6.  Obesity and thyroid function.

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Review 10.  The Global Epidemic of the Metabolic Syndrome.

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  2 in total

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2.  Augmented Production of Platelets From Cord Blood With Euchromatic Histone Lysine Methyltransferase Inhibition.

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  2 in total

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