VRK-1 extends life span by activation of AMPK via phosphorylation
SCIE
SCOPUS
- Title
- VRK-1 extends life span by activation of AMPK via phosphorylation
- Authors
- Park, Sangsoon; Artan, Murat; Han, Seung Hyun; Park, Hae-Eun H.; Jung, Yoonji; Hwang, Ara B.; Shin, Won Sik; Kim, Kyong-Tai; Lee, Seung-Jae, V
- Date Issued
- 2020-07
- Publisher
- AMER ASSOC ADVANCEMENT SCIENCE
- Abstract
- Vaccinia virus-related kinase (VRK) is an evolutionarily conserved nuclear protein kinase. VRK-1, the single Caenorhabditis elegans VRK ortholog, functions in cell division and germline proliferation. However, the role of VRK-1 in postmitotic cells and adult life span remains unknown. Here, we show that VRK-1 increases organismal longevity by activating the cellular energy sensor, AMP-activated protein kinase (AMPK), via direct phosphorylation. We found that overexpression of vrk-1 in the soma of adult C. elegans increased life span and, conversely, inhibition of vrk-1 decreased life span. In addition, vrk-1 was required for longevity conferred by mutations that inhibit C. elegans mitochondria! respiration, which requires AMPK. VRK-1 directly phosphorylated and up-regulated AMPK in both C. elegans and cultured human cells. Thus, our data show that the somatic nuclear kinase, VRK-1, promotes longevity through AMPK activation, and this function appears to be conserved between C. elegans and humans.
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/104104
- DOI
- 10.1126/sciadv.aaw7824
- ISSN
- 2375-2548
- Article Type
- Article
- Citation
- SCIENCE ADVANCES, vol. 6, no. 27, 2020-07
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- There are no files associated with this item.
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