Recognition of Cytosolic DNA Attenuates Glucose Metabolism and Induces AMPK Mediated Energy Stress Response

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Recognition of Cytosolic DNA Attenuates Glucose Metabolism and Induces AMPK Mediated Energy Stress Response

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Title: Recognition of Cytosolic DNA Attenuates Glucose Metabolism and Induces AMPK Mediated Energy Stress Response
Author: Zheng, Min; Xie, Linna; Liang, Yaoji; Wu, Suqin; Xu, Huijuan; Zhang, Yuedong; Liu, Hekun; Lin, Dexin; Han, Jiahuai; Lu, Kunping

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Citation: Zheng, Min, Linna Xie, Yaoji Liang, Suqin Wu, Huijuan Xu, Yuedong Zhang, Hekun Liu, Dexin Lin, Jiahuai Han, and Kunping Lu. 2015. “Recognition of Cytosolic DNA Attenuates Glucose Metabolism and Induces AMPK Mediated Energy Stress Response.” International Journal of Biological Sciences 11 (5): 587-594. doi:10.7150/ijbs.10945. http://dx.doi.org/10.7150/ijbs.10945.
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Abstract: Both viral infection and DNA transfection expose single-stranded or double-stranded DNA to the cytoplasm of mammalian cells. Recognition of cytosolic DNA activates a series of cellular responses, including induction of pro-inflammatory genes such as type I interferon through the well-known cGAS-STING pathway. Here we show for the first time that intracellular administration of either single or double stranded interferon stimulating DNA (ISD), but not poly(dA) suppresses cell growth in many different cell types. Suppression of cell growth by cytosolic DNA is cGAS/STING independent and associated with inhibition of glucose metabolism, ATP depletion and subsequent cellular energy stress responses including activation of AMPK and inactivation of mTORC1. Our results suggest that in concert with but independent of innate immune response, recognition of cytosolic DNA induced cellular energy stress potentially functions as a metabolic barrier to viral replication.
Published Version: doi:10.7150/ijbs.10945
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4400389/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:15035060
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