The Rps23rg gene family originated through retroposition of the ribosomal protein s23 mRNA and encodes proteins that decrease Alzheimer's beta-amyloid level and tau phosphorylation.

Human Molecular Genetics
Xiumei HuangYun-wu Zhang

Abstract

Retroposition is an important mechanism for gene origination. However, studies to elucidate the functions of new genes originated through retroposition, especially the functions related to diseases, are limited. We recently identified a mouse gene, Rps23 retroposed gene 1 (Rps23rg1), that regulates beta-amyloid (Abeta) level and tau phosphorylation, two major pathological hallmarks of Alzheimer's disease (AD), and found that Rps23rg1 originated through retroposition of the mouse ribosomal protein S23 (Rps23) mRNA. Here we show that retroposition of Rps23 mRNA occurred multiple times in different species but only generated another functionally expressed Rps23rg1-homologous gene, Rps23rg2, in mice, whereas humans may not possess functional Rps23rg homologs. Both Rps23rg1 and Rps23rg2 are reversely transcribed relative to the parental Rps23 gene, expressed in various tissues and encode proteins that interact with adenylate cyclases. Similar to the RPS23RG1 protein, RPS23RG2 can upregulate protein kinase A activity to reduce the activity of glycogen synthase kinase-3, Abeta level and tau phosphorylation. However, the effects of RPS23RG2 are weaker than those of RPS23RG1 and such a difference could be attributed to the extra carboxy...Continue Reading

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Citations

Mar 5, 2011·Molecular Neurodegeneration·Young-Don KwakFrancesca-Fang Liao
Aug 17, 2012·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Yaomin ChenHuaxi Xu
Jan 7, 2016·Scientific Reports·Li YanHuaxi Xu
Mar 24, 2015·PloS One·Peng-Rong CaoYuan Lv
Mar 9, 2019·Reviews in the Neurosciences·Caitlin NyhusVanessa Jane Hall
Sep 11, 2020·Cell Death and Differentiation·Dongdong ZhaoYun-Wu Zhang

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