自噬作用可幫助細胞清除廢物和異物,，維持健康,。日本研究人員最新發(fā)現(xiàn)兩種能促進或阻礙細胞自噬作用的蛋白質(zhì),，它們對自噬作用而言就好似“油門”或“剎車”,。
大阪大學(xué)教授吉森保領(lǐng)導(dǎo)的研究小組以承擔(dān)細胞自噬作用的蛋白質(zhì)Beclin為對象研究發(fā)現(xiàn),，如果Beclin與蛋白質(zhì)Atg14L結(jié)合,，自噬作用就會增強；如果Beclin與另外一種蛋白質(zhì)Rubicon結(jié)合，自噬作用就會減弱,。
研究人員認為,，Atg14L和Rubicon以一種復(fù)雜機制保持平衡，一旦這種平衡被打破,，就有可能誘發(fā)癌癥,。因此，這兩種蛋白質(zhì)保持平衡有助于阻止癌變,。
這一研究成果已發(fā)表在最新一期英國《自然·細胞生物學(xué)》雜志網(wǎng)絡(luò)版上,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
