PI3K突變 (p85β) 強化抗氧化與 延壽20％

日發現新長壽基因 可延長生命20％ 或還可防糖尿病癌症 2019/09/17 中時 施施 糖尿病和部分癌症被認為與肥胖有關。日本岡山縣高梁市私立吉備國際大學的加納良男教授12日在記者會上宣布，發現1種新的突變基因。這種基因除可讓肥胖的實驗對象老鼠延壽20％，甚至可能具有預防糖尿病及抑制癌症的功能。相關論文本月初刊於英國期刊《科學報告》（Science Reports）。這種新發現的基因名為「變異p85β」，由有分泌胰島素功能的基因突變而成。加納教授發現注入新基因的實驗鼠比沒有注射的多活4個月，前者對與老化有關的活性氧類（ROS）的抵抗力，是後者的20倍。由於新的基因可促進胰島素分泌及抑制癌細胞增生，也有助讓實驗鼠的血糖值保持穩定，外界期待這樣的發現可用於未來研發糖尿及癌症藥物。加納教授表示：「這項研究花了足足15年時間，很感謝校方對我的支持。」(中時 )

C-SH2 point mutation converts p85β regulatory subunit of phosphoinositide 3-kinase to an anti-aging gene  Scientific Reportsvolume 9, Article number: 12683 (2019)

Insulin interacts with the insulin receptor, and the activated receptor promotes activity of the phosphoinositide-3 kinase (PI3K) enzyme. A decrease in insulin or insulin-like growth factor 1 (IGF-1) signaling increases the lifespan in mammalian species. We found that a point mutation in the C-SH2 domain of the p85β regulatory subunit of PI3K results in a prolonged lifespan. In p85β mutant cells, nerve growth factor (NGF) activates the longevity protein FOXO, and the mutant p85β gene produces strong resistance to oxidative stress, which contributes to aging. The p85β gene mutation causes increased serum insulin and low blood glucose in p85β mutant transgenic mice. Our results indicate that the p85β mutant allele alters the activity of downstream targets of PI3K by NGF and platelet-derived growth factor (PDGF) but not by insulin. We report that a point mutation in the C-SH2 domain of p85β transforms p85β into a novel anti-aging gene by abnormally regulating PI3K.