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林圣彩教授博导

发布时间:2015-11-30来源:点击数:29061

林圣彩教授博士生导师LIN Shengcai, Ph.D.

长江学者特聘教授,博士生导师

课题组组长

  话:+86-592-2182993

E-maillinsc@xmu.edu.cn

http://linlab.xmu.edu.cn

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;

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

1995-2001年,新加坡国立大学分子与细胞生物研究所,实验室主任;

2001-2006年,香港科技大学生化系助理教授、副教授(获终身职位);兼职于厦门大学生命科学学院,任长江学者特聘教授;

200312-20175月,任厦门大学生命科学学院院长;

20066月至今,厦门大学生命科学学院,教授、博士生导师。


1984, B.S. 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;

2003.12-2017.5, Dean, School of Life Sciences, Xiamen University;

2006.6 to Present, Professor, Cheung Kong Scholar, Xiamen University.


 

研究领域(Research Area)

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。  

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. We have also revealed that the ULK kinases phosphorylate multiple glycolytic enzymes and regulate glucose metabolic fluxes dependently of autophagy.

   The main focus of our research has also been on the mechanisms for the regulation of the AMP-activated protein kinase. We have shown that the lowenergy signal AMP can autonomously initiate assembly of an activating complex for the energy sensor kinase AMPK, in that the scaffold protein AXIN tethers LKB1 to AMPK. Moreover, we have found that the AXIN/LKB1/AMPK complex and mTORC1 inversely utilize the common v-ATPaseRagulator complex for activation on the surface of lysosome, thereby uncovering a switch between anabolism and catabolism. We are exploring further how AMPK and its activating kinase LKB1 are regulated and the biological functions of these kinases.



代表性论文(Selected Publications)

1.    Zhang CS, Li MQ, Ma T, Zong Y, Cui JW, Feng JW, Wu YQ, Lin SY, Lin SC*. Metformin Activates AMPK through the Lysosomal Pathway. Cell Metabolism, 24(4)(2016), 521-522.

2.    Li YT, Sun Y, Liang Y, Liu Q, Shi YZ, Zhang CS, Zhang CX, Song LT, Zhang P, Zhang XZ, Li XT, Chen T, Huang HY, He XD, Wang Y, Wu YQ, Chen SX, Jiang M, Chen CH, Xie CC, James Y. Yang, Lin Y, Zhao SM, Ye ZY, Lin SY, Daniel Tsun-yee Chiu, Lin SC*. ULK1/2 Constitute a Bifurcate Node Controlling Glucose Metabolic Fluxes in Addition to Autophagy. Molecular Cell, 62(3)(2016), 359-370.

3.    Zhang CS, Lin SC*. AMPK Promotes Autophagy by Facilitating Mitochondrial Fission. Cell Metabolism, 23(3)(2016), 399-401.

4.    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(3)(2014), 526-540.

5.    Zhang YL, Guo HL, Zhang CS, Lin SY, Li P, Wu JW, Lin SC*. AMP as a low energy charge signal autonomously initiates assembly of AXIN-AMPK-LKB1 complex for AMPK activation. Cell Metabolism, 18(4)(2013), 546-555.

6.    Lin SY, Li TY, Liu Q, Zhang CS, Li X, Chen Y, Zhang SM, Lian GL, Liu Q, Ruan K, Wang Z, Zhang CS, Chien KY, Wu J, Li QX, Han JH, Lin SC*. GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy. Science, 336(6080)(2012), 477-481.

7.    Li QX, Lin SY, Wang X, Lian GL, Lu ZL, Guo HL, Ruan K, Wang YH, Ye ZY, Han JH, Lin SC*. Axin determines cell fate by controlling the p53 activation threshold after DNA damage. Nature Cell Biology, 11(9)(2009), 1128-1135.

8.    Rui YN, Xu Z, Xiong B, Cao Y, Lin SY, Chan SC, Luo W, Han Y, Lu ZL, Ye ZY, Zhou HM, Han JH, Meng A*, Lin SC*. A ß-catenin-independent dorsalization pathway activated by Axin/JNK signaling and antagonized by Aida. Developmental Cell, 13(2)(2007), 268-282.

9.    Rui YN, Xu Z, Lin SY, Li QX, Rui HL, Luo W, Zhou HM, Cheung PY, Wu ZG, Ye ZY, Li P, Han JH, Lin SC*. Axin stimulates p53 functions by activation of HIPK2 kinase through multimeric complex formation. The EMBO Journal. 23(23)(2004), 4583-4594.