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Int. J. Mol. Sci. 2013, 14(9), 19202-19229; doi:10.3390/ijms140919202

Posttranscriptional Regulation of Insulin Family Ligands and Receptors

Laboratory of Genetics, National Institute on Aging-Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
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Received: 3 July 2013 / Revised: 17 August 2013 / Accepted: 6 September 2013 / Published: 18 September 2013
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Abstract

Insulin system including ligands (insulin and IGFs) and their shared receptors (IR and IGFR) are critical regulators of insulin signaling and glucose homeostasis. Altered insulin system is associated with major pathological conditions like diabetes and cancer. The mRNAs encoding for these ligands and their receptors are posttranscriptionally controlled by three major groups of regulators; (i) alternative splicing regulatory factors; (ii) turnover and translation regulator RNA-binding proteins (TTR-RBPs); and (iii) non-coding RNAs including miRNAs and long non-coding RNAs (lncRNAs). In this review, we discuss the influence of these regulators on alternative splicing, mRNA stability and translation. Due to the pathological impacts of insulin system, we also discussed the possibilities of discovering new potential regulators which will improve understanding of insulin system and associated diseases. View Full-Text
Keywords: glucose homeostasis; insulin-like growth factor; insulin-like growth factor receptor; RNA-binding protein; micro RNA; long noncoding RNA; mRNA decay; mRNA translation; insulin signaling; alternative splicing IRES glucose homeostasis; insulin-like growth factor; insulin-like growth factor receptor; RNA-binding protein; micro RNA; long noncoding RNA; mRNA decay; mRNA translation; insulin signaling; alternative splicing IRES
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Panda, A.C.; Grammatikakis, I.; Yoon, J.-H.; Abdelmohsen, K. Posttranscriptional Regulation of Insulin Family Ligands and Receptors. Int. J. Mol. Sci. 2013, 14, 19202-19229.

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