한빛사논문
- 조회1,340
POSTECH
Sangsoon Park1,*, Murat Artan1,*,†, Seung Hyun Han2,*, Hae-Eun H. Park3, Yoonji Jung3, Ara B. Hwang1,‡, Won Sik Shin2, Kyong-Tai Kim1,2,§ and Seung-Jae V. Lee3,§
1Department of Life Sciences, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, South Korea.
2Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Gyeongbuk 37673, South Korea.
3Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, South Korea.
§Corresponding author.
*These authors contributed equally to this work.
†Present address: Institute of Science and Technology (IST) Austria, Am Campus 1, Klosterneuburg 3400, Austria.
‡Present address: Memphis Meats Inc., P.O. Box 3468, Berkeley, CA 94703, USA.
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.
논문정보
TOP52020년 후보
- Research article
- 2020년 07월 (BRIC 등록일 2020-07-07)
- 국내 연구진
- 생명과학 > 노화/암생물학
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