自噬
颗粒(地质)
细胞生物学
PI3K/AKT/mTOR通路
胰岛素
生物
调节器
营养感应
β细胞
化学
内科学
内分泌学
生物化学
信号转导
细胞凋亡
医学
基因
古生物学
小岛
作者
Alexander Goginashvili,Zhirong Zhang,Eric Erbs,Coralie Spiegelhalter,Pascal Kessler,Michael Mihlan,Adrien Pasquier,Ksenia Krupina,Nicole L. Schieber,Laura Cinque,Joëlle Morvan,Izabela Sumara,Yannick Schwab,Carmine Settembre,Roméo Ricci
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2015-02-20
卷期号:347 (6224): 878-882
被引量:141
标识
DOI:10.1126/science.aaa2628
摘要
Too hungry to eat, too hungry not to eat Pancreatic beta cells, the source of insulin in response to food, employ an unusual mechanism to adapt to nutrient depletion. Goginashvili et al. found that starvation of beta cells induced selective degradation of newly formed insulin granules through their fusion with lysosomes, the cell's garbage disposal units (see the Perspective by Rutter). The nutrient sensor mTOR is recruited to these lysosomes, leading to its local activation and the suppression of autophagy—a process by which cells “eat” their own constituents. Protein kinase D, a major regulator of insulin granule biogenesis, controls this granule degradation in response to nutrient availability. Thus, unlike most other cells, autophagy is not the strategy of choice in beta cells to adapt to starvation. Science , this issue p. 878 ; see also p. 826
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