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林圣彩教授 博导
出处: 发布时间:2016-10-02 浏览次数:235

林圣彩教授博士生导师林圣彩  LIN Shengcai, Ph.D.

教授, 博士生导师

调节生物学Regulatory Biology

课题组组长

话:+86-592-2182993

E-maillinsc@xmu.edu.cn

http://121.192.179.196/linlab/


1984年,厦门大学生物系,学士学位;

1991年,美国德克萨斯大学西南医学中心,生物化学博士;

1991年至1995年,美国Howard Hughes Institute at UCSD博士后;

1995年至2001年,新加坡国立大学分子与细胞生物研究所实验室主任;

2001年至2006年,香港科技大学生化系助理教授、副教授;兼职于厦门大学生命科学学院,任长江学者特聘教授;2003年起出任院长;

2006年至今,厦门大学生命科学学院长江学者、博士生导师。


1984, B.Sc. Xiamen University;

1991, Ph.D., UT Southwestern Medical Center at Dallas;

1991-1995, Postdoctoral Fellow at the Howard Hughes Medical Institute, UCSD;

1995-2001, Principal Investigator, IMCB, Singapore;

2001-2006, Assistant Professor/Associate Professor (tenured), Hong Kong University of Science and Technology; 2003 to Present, Dean, School of Life Sciences, Xiamen University.

2001 to Present, Professor, Cheung Kong Scholar, Xiamen University.


研究领域(Research Area)

Our research lies in the broad area of the molecular mechanisms that underlie metabolic homeostasis and its relationship to cell growth control. We have discovered a signaling pathway comprising the protein kinase GSK3, acetyltransferase TIP60, and protein kinase ULK1, which activates autophagy in cells deprived of serum, elucidating the molecular mechanism linking nutritional starvation to autophagy. More recently, we have that the low-energy signal AMP can autonomously initiate assembly of an activating complex for the energy sensor kinase AMPK. Current interests include further exploration of how AMPK is regulated at the molecular biology, subcellular organelle, and organismal levels, and study of how the autophagy cross-talks to the overall metabolic control or reprogramming. Our ultimate goal is to reveal a unifying mechanism that governs metabolic homeostasis in response to metabolic stresses, and the metabolic checkpoint for cell growth.

本课题的研究兴趣在于细胞代谢稳态维持及其调控细胞生长的分子机制。我们之前发现了由GSK3激酶、乙酰转移酶TIP60ULK1激酶组成的一条介导细胞在缺乏生长因子时诱导细胞自噬的信号转导通路。新近又发现了细胞在缺乏能量时所积累的AMP能自主地诱导一个基于Axin的蛋白质复合体的形成来激活能量感受激酶AMPK,在能量平衡的机制方面做出了一个重大发现。我们将基于上述介导细胞自噬和能量平衡的分子机制的发现,继续开展细胞维持代谢稳态的生物学研究,包括自噬通路与细胞整体代谢调控的交叉的机制,在分子、细胞器、个体多水平上研究细胞代谢稳态调控与细胞生长的关系。


代表性论文(Selected Publications)

  1. Zhang CS, Jiang B,Li MQ, Zhu MJ, Peng YY, Zhang YL, Wu YQ, Li TY, Liang Y, Lu ZL, Lian GL, Liu Q, Guo HL,Yin ZY, Ye ZY, Han J, Wu JW, Yin HY, Lin SY, Lin SC*. The lysosomal v-ATPase-ragulator complex is a common activator for AMPK and mTORC1, Acting as a switch between catabolism and anabolism. Cell Metabolism, 20, 526-540, 2014

  2. Zhang YL, Guo HL, Zhang CS, Lin SY, Li P, WU JW, and Lin SC*. AMP as a low energy charge signal autonomously initiates assembly of AXIN-AMPK-LKB1 complex for AMPK activation. Cell Metabolism 18, 546–555, 2013

  3. Lin SY, Li TY, Liu Q, Zhang C, Li X, Chen Y,  Zhang SM, Lian G, Liu Q, Ruan K, Wang Z, Zhang CS, Chien KY, Wu J, Li Q, Han J, and Lin SC*. Protein phosphorylation-acetylation cascade connects growth factor deprivation to autophagy. Autophagy, 8(9):1385-6, 2012

  4. Guo HL, Zhang C, Liu Q, Li Q, Lian G, Wu D, Li X, Zhang W, Shen Y, Ye Z, Lin SY, Lin SC*. The Axin/TNKS complex interacts with KIF3A and is required for insulin-stimulated GLUT4 translocation. Cell Res. 22: 1246-57, 2012

  5. Lin SY, Li TY, Liu Q, Zhang C, Li X, Chen Y,  Zhang SM, Lian G, Liu Q, Ruan K, Wang Z, Zhang CS, Chien KY, Wu J, Li Q, Han J, and Lin SC*. GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy. Science 336, 477, 2012

  6. Li, Q., He, Y., Wu, X., Wei, L., Lin, S.-Y., Wang, Z., Lin, S.-C*. AXIN is an essential co-activator for the promyelocytic leukemia protein in p53 activation. Oncogene 30: 1194-1204, 2011.

  7. Li, Q., Lin, S.Y., Wang, X., Lian, G., Lu. Z., Guo, H., Ruan, K., Wang, Y., Ye, Z., Han, J., and Lin, S-C*. Axin determines cell fate by controlling the p53 activation threshold after DNA damage. Nat. Cell Biol. 11, 1128-1135, 2009.

  8. Lu, Z., Liu, W., Huang, H., He, Y., Han, Y., Wang, Y., Li, Q., Ruan, K., Ye, Z., Low, B. C., Meng, A., Lin, S.-C*. Protein encoded by the AxinFu allele effectively downregulates Wnt signaling but exerts a dominant negative effect on c-Jun N-terminal kinase signaling. J. Biol. Chem. 283, 13132-9, 2008.

  9. Li, Q., Wang, X., Wu, X., Rui, Y., Liu, W., Wang, J., Wang, X., Liou, Y.-C., Ye, Z., and Lin, S.-C. Daxx cooperates with the Axin/HIPK2/p53 complex to induce cell death. Cancer Res., 67, 66-74, 2007.

  10. Rui, Y., Xu, Z., Xiong, B., Cao, Y., Lin, S., Chan, S.C., Luo, W., Han, Y., Lu, Z., Ye, Z., Zhou, H.-M., Han, J., Meng, A.*, Lin, S.-C.* A ß-catenin-independent dorsalization pathway activated by Axin/JNK signaling and antagonized by Aida. Dev. Cell, 13, 268-282, 2007.

  11. Rui,Y.N., Xu, Z., Lin, S.Y., Li, Q.X., Rui, H.L., Luo, W., Zhou, H.M., Cheung, P.Y., Wu, Z.G., Ye, Z.Y., Li, P., Han, J.H., and Lin, S.-C.*  Axin stimulates p53 functions by activation of HIPK2 kinase through multimeric complex formation. EMBO J. 23, 4583-4594, 2004

  12. Rui,Y.N., Xu, Z., Lin, S.Y., Li, Q.X., Rui, H.L., Luo, W., Zhou, H.M., Cheung, P.Y., Wu, Z.G., Ye, Z.Y., Li, P., Han, J.H., and Lin, S.-C.*  Axin stimulates p53 functions by activation of HIPK2 kinase through multimeric complex formation. EMBO J. 23, 4583-4594, 2004

Lab Associates

Ms. Zhiyun Ye (叶志云), Research scientist

Dr. Shuyong Lin (林舒勇), Assistant Professor

Dr. Zheng Ying (郑颖), Associate Researcher