自噬作用可帮助细胞清除废物和异物，维持健康。日本研究人员最新发现两种能促进或阻碍细胞自噬作用的蛋白质，它们对自噬作用而言就好似“油门”或“刹车”。
大阪大学教授吉森保领导的研究小组以承担细胞自噬作用的蛋白质Beclin为对象研究发现，如果Beclin与蛋白质Atg14L结合，自噬作用就会增强；如果Beclin与另外一种蛋白质Rubicon结合，自噬作用就会减弱。
研究人员认为，Atg14L和Rubicon以一种复杂机制保持平衡，一旦这种平衡被打破，就有可能诱发癌症。因此，这两种蛋白质保持平衡有助于阻止癌变。
这一研究成果已发表在最新一期英国《自然·细胞生物学》杂志网络版上。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Cell Biology 8 March 2009 | doi:10.1038/ncb1846
Two Beclin 1-binding proteins, Atg14L and Rubicon, reciprocally regulate autophagy at different stages
Kohichi Matsunaga1,2, Tatsuya Saitoh3,4, Keisuke Tabata1, Hiroko Omori1, Takashi Satoh3,4, Naoki Kurotori1, Ikuko Maejima1, Kanae Shirahama-Noda1, Tohru Ichimura5, Toshiaki Isobe5, Shizuo Akira3,4, Takeshi Noda1 & Tamotsu Yoshimori1,6
AbstractBeclin 1, a protein essential for autophagy, binds to hVps34/Class III phosphatidylinositol-3-kinase and UVRAG. Here, we have identified two Beclin 1 associated proteins, Atg14L and Rubicon. Atg14L and UVRAG bind to Beclin 1 in a mutually exclusive manner, whereas Rubicon binds only to a subpopulation of UVRAG complexes; thus, three different Beclin 1 complexes exist. GFP–Atg14L localized to the isolation membrane and autophagosome, as well as to the ER and unknown puncta. Knockout of Atg14L in mouse ES cells caused a defect in autophagosome formation. GFP–Rubicon was localized at the endosome/lysosome. Knockdown of Rubicon caused enhancement of autophagy, especially at the maturation step, as well as enhancement of endocytic trafficking. These data suggest that the Beclin 1–hVps34 complex functions in two different steps of autophagy by altering the subunit composition.
1 Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, 3-1Yamadaoka, Suita, Osaka 565-0871, Japan.
2 Department of Genetics, The Graduate University for Advanced Studies, Mishima 455-8540, Japan.
3 Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1Yamadaoka, Suita, Osaka 565-0871, Japan.
4 Department of Host Defense, Research Institute for Microbial Diseases. Osaka University, 3-1Yamadaoka, Suita, Osaka 565-0871, Japan.
5 Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji, Tokyo 192-0397, Japan.
6 CREST, Japan Science and Technology Agency, Kawaguchi-Saitama 332-0012, Japan.
