교수 및 연구

리서치하이라이트
리서치하이라이트

VRK-1 extends life span by activation of AMPK via phosphorylation

  • 저널명SCIENCE ADVANCES
    • 담당교수Kyong-Tai Kim
    • 조회295
    • 작성자최고관리자
    • 2020-07-06

    본문

    c45a585d3fd65b5cf93810a17d9b43e8_1594014436_9176.jpg
    ■ 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