宋保亮 - 武汉大学 - 生命科学学院

个人简介

教育经历 1993-1997 南京大学生物科学与技术系，学士 1997-2002 中科院上海生命科学研究院生物化学与细胞生物学研究所，博士工作经历与任职 2002-2005　美国德克萨斯大学西南医学中心，博士后 2005-2014　中科院上海生命科学研究院生物化学与细胞生物学研究所，研究员其中：2012-2014 分子生物学国家重点实验室副主任 2013-2014 生化细胞所所长助理 2014-至今　武汉大学生命科学学院，教授、院长

研究领域

1）首次发现并证明溶酶体通过和过氧化物酶体形成膜接触将胆固醇转移给后者，开拓了胆固醇运输研究的前沿领域；2）系统性阐明小肠胆固醇吸收的分子途径，鉴定出该途径中一系列重要蛋白；3）深入探索胆固醇内源合成的负反馈调控机制—HMGCR蛋白的受控降解，揭示肝脏脂质合成与脂肪能量代谢的联系；4）构建基于胆固醇合成负反馈调控途径的筛选体系，获得能同时降低胆固醇和甘油三酯的活性化合物—白桦酯醇；5）发现抑制胆固醇合成可明显减少肝癌发生，以及胆固醇可共价修饰SMO蛋白，揭示胆固醇代谢的新功能。

近期论文

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1. Zhang YY, Fu ZY, Wei J, Qi W, Baituola G, Luo J, Meng YJ, Guo SY, Yin H, Jiang SY, Li YF, Miao HH, Liu Y, Wang Y, Li BL, Ma YT*, Song BL* (2018). A LIMA1 variant promotes low plasma LDL cholesterol and decreases intestinal cholesterol absorption. Science 360(6393):1087-1092. 2. Wang YJ, Bian Y, Luo J, Lu M, Xiong Y, Guo SY, Yin HY, Lin X, Li Q, Chang CCY, Chang TY, Li BL*, Song BL* (2017). Cholesterol and fatty acids regulate cysteine ubiquitylation of ACAT2 through competitive oxidation. Nature Cell Biology 19(7):808-819. 3. Xiao X, Tang JJ, Peng C, Wang Y, Fu L, Qiu ZP, Xiong Y, Yang LF, Cui HW, He XL, Yin L, Qi W, Wong CL, Zhao Y, Li BL, Qiu WW*, Song BL* (2017). Cholesterol modification of Smoothened is required for hedgehog signaling. Molecular Cell 66(1):1-9. 4. Li N, Zhou ZS, Shen Y, Xu J, Miao HH, Xiong Y, Xu F, Li BL, Luo J, Song BL* (2017). Inhibition of the SREBP pathway suppresses hepatocellular carcinoma through repressing inflammation. Hepatology 65(6): 1936-1947. 5. Xie C, Zhang YP, Song L, Luo J, Qi W, Hu J, Lu D, Yang Z, Zhang J, Xiao J, Zhou B, Du JL, Jing N, Liu Y, Wang Y, Li BL, Song BL*, Yan Y* (2016). Genome editing with CRISPR/Cas9 in postnatal mice corrects PRKAG2 cardiac syndrome. Cell Research 26(10):1099-1111. 6. Chu BB, Liao YC, Qi W, Xie C, Du X, Wang J, Yang H, Miao HH, Li BL, Song BL* (2015). Cholesterol transport through lysosome-peroxisome membrane contacts. Cell 161(2):291-306. 7. Li PS, Fu ZY, Zhang YY, Zhang JH, Xu CQ, Ma YT, Li BL, Song BL* (2014). The clathrin adaptor Numb regulates intestinal cholesterol absorption through dynamic interaction with NPC1L1. Nature Medicine 20(1):80-6. 8. Liu TF, Tang JJ, Li PS, Shen Y, Li JG, Miao HH, Li BL*, Song BL* (2012). Ablation of gp78 in liver improves hyperlipidemia and insulin resistance by inhibiting SREBP to decrease lipid biosynthesis. Cell Metabolism 16(2):213-25. 9. Tang JJ, Li JG, Qi W, Qiu WW, Li PS, Li BL, Song BL* (2011). Inhibition of SREBP by a small molecule, betulin, improves hyperlipidemia and insulin resistance and reduces atherosclerotic plaques. Cell Metabolism 13(1):44-56. 10. Ge L, Qi W, Wang LJ, Miao HH, Qu YX, Li BL, Song BL* (2011). Flotillins play an essential role in Niemann-Pick C1-like 1-mediated cholesterol uptake. Proc Natl Acad Sci U S A 108(2):551-6. 11. Ge L, Wang J, Qi W, Miao HH, Cao J, Qu YX, Li BL, Song BL* (2008). The cholesterol absorption inhibitor ezetimibe acts by blocking the sterol-induced internalization of NPC1L1. Cell Metabolism 7(6):508-19. 12. Cao J, Wang J, Qi W, Miao HH, Wang J, Ge L, DeBose-Boyd RA, Tang JJ, Li BL*, Song BL* (2007). Ufd1 is a cofactor of gp78 and plays a key role in cholesterol metabolism by regulating the stability of HMG-CoA reductase. Cell Metabolism 6(2):115-28. 13. Song BL, Sever N, DeBose-Boyd RA (2005). Gp78, a membrane-anchored ubiquitin ligase, associates with Insig-1 and couples sterol-regulated ubiquitination to degradation of HMG CoA reductase. Molecular Cell 19(6):829-40. 14. Song BL, Javitt NB, DeBose-Boyd RA (2005). Insig-mediated degradation of HMG CoA reductase stimulated by lanosterol, an intermediate in the synthesis of cholesterol. Cell Metabolism 1(3):179-89.