東北大学加齢医学研究所 加齢医学研究拠点 | Institute of Development, Aging and Cancer, Tohoku University

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◇平成28年3月7日(月)加齢研セミナ-のご案内
日時: 平成28年3月7日(月)午後5時~
場所: 加齢研実験研究棟7階 セミナー室1
演題: Metabolic homeostasis, redox signaling, and aging
講師: Keith Blackwell
所属: Joslin Diabetes Center 
Harvard Medical School Department of Genetics
担当: 本橋 ほづみ(遺伝子発現制御分野・内線8550)
要旨: In the nematode C. elegans, the Nrf/CNC proteins are represented by their ortholog SKN-1. SKN-1 exhibits remarkable functional conservation with mammalian Nrf/CNC proteins, suggesting that C. elegans may have considerable predictive value for investigating how Nrf/CNC proteins function and are regulated. Our work in C. elegans indicates that SKN-1 regulation is surprisingly complex, and is influenced by numerous growth, nutrient, and metabolic signals. We also find that SKN-1 is essential in most pathways capable of extending C. elegans lifespan and healthspan. Two recent studies provide new insights into SKN-1 functions and regulation. We find that SKN-1 plays a major role in lipid metabolism, and seems to be regulated by lipid signals. We also have determined that the endoplasmic reticulum (ER) transmembrane protein IRE-1 functions as a redox-regulated sentinel that activates p38 and SKN-1 in response to certain cytoplasmic stresses. This pathway is conserved in humans, in which it regulates the SKN-1 homolog Nrf2. Our data indicate that the ER functions as a sentinel that monitors stress in the cytoplasm, as well as within the secretory pathway.


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