@article{15057,
  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 mitochondrial 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.},
  author       = {Park, Sangsoon and Artan, Murat and Han, Seung Hyun and Park, Hae-Eun H. and Jung, Yoonji and Hwang, Ara B. and Shin, Won Sik and Kim, Kyong-Tai and Lee, Seung-Jae V.},
  issn         = {2375-2548},
  journal      = {Science Advances},
  number       = {27},
  publisher    = {American Association for the Advancement of Science},
  title        = {{VRK-1 extends life span by activation of AMPK via phosphorylation}},
  doi          = {10.1126/sciadv.aaw7824},
  volume       = {6},
  year         = {2020},
}