Cytoplasmic Polyadenylation Element Binding Protein Deficiency Stimulates PTEN and Stat3 mRNA Translation and Induces Hepatic Insulin Resistance

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Cytoplasmic Polyadenylation Element Binding Protein Deficiency Stimulates PTEN and Stat3 mRNA Translation and Induces Hepatic Insulin Resistance

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Title: Cytoplasmic Polyadenylation Element Binding Protein Deficiency Stimulates PTEN and Stat3 mRNA Translation and Induces Hepatic Insulin Resistance
Author: Alexandrov, Ilya M.; Ivshina, Maria; Jung, Dae Young; Friedline, Randall; Ko, Hwi Jin; Xu, Mei; O'Sullivan-Murphy, Bryan; Bortell, Rita; Huang, Yen-Tsung; Urano, Fumihiko; Kim, Jason Hwan; Richter, Joel D.

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Citation: Alexandrov, Ilya M., Maria Ivshina, Dae Young Jung, Randall Friedline, Hwi Jin Ko, Mei Xu, Bryan O'Sullivan-Murphy, Rita Bortell, Yen-Tsung Huang, Fumihiko Urano, Jason K. Kim, and Joel D. Richter. 2012. Cytoplasmic polyadenylation element binding protein deficiency stimulates pten and stat3 mrna translation and induces hepatic insulin resistance. PLoS Genetics 8(1).
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Abstract: The cytoplasmic polyadenylation element binding protein CPEB1 (CPEB) regulates germ cell development, synaptic plasticity, and cellular senescence. A microarray analysis of mRNAs regulated by CPEB unexpectedly showed that several encoded proteins are involved in insulin signaling. An investigation of Cpeb1 knockout mice revealed that the expression of two particular negative regulators of insulin action, PTEN and Stat3, were aberrantly increased. Insulin signaling to Akt was attenuated in livers of CPEB–deficient mice, suggesting that they might be defective in regulating glucose homeostasis. Indeed, when the Cpeb1 knockout mice were fed a high-fat diet, their livers became insulin-resistant. Analysis of HepG2 cells, a human liver cell line, depleted of CPEB demonstrated that this protein directly regulates the translation of PTEN and Stat3 mRNAs. Our results show that CPEB regulated translation is a key process involved in insulin signaling.
Published Version: doi:10.1371/journal.pgen.1002457
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257279/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11211543
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