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全所PI名录 >

 
林安宁
研究员(客座),研究组长,博士生导师
E-mail: alin@@sibcb.ac.cn

研究方向

信号转导与基因调控


研究工作
癌症信号转导网络与基因调控的分子机理
        细胞信号转导(signal transduction)在诸如增殖、分化、程序性死亡、转化等细胞活动的调控中都扮演了至关重要的角色。信号转导调控的异常(deregulation)会导致很多人类疾病甚至癌症。细胞外的各种信号通过一个由众多信号转导通路构成的细胞内信号转导网络(intracellular signaling network)传输到细胞内部,从而调控至关重要的细胞活动。虽然细胞内信号转导网络结构已经相当清楚,但信号网络在人体内的生物学作用与调控尚有待进一步研究。本实验室的工作主要是利用c-Jun N-terminal protein kinase (JNK)和IkB kinase(IKK)/NF-kappaB等分子探针来研究决定信号转导网络的可塑性(plasticity)和特异性(specificity)的分子机制,以试图理解信号转导网络调控的异常怎样导致人类疾病和癌症。
        更多细节请参看:http://ben-may.bsd.uchicago.edu/faculty/lin.htm


代表性论文

  1. Lin A, Frost J, Deng T, Smeal T, Al-Alawi N, Kikkawa U, Hunter T, Brenner A, and Karin M. Casein kinase II is a negative regulator of c-Jun DNA binding and AP-1 activity. Cell. 70:777-789, 1992.
  2. Hibi M, Lin A, Smeal T, Minden A, and Karin M. Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. Genes & Development 7:2135-2148, 1993.
  3. Minden A, Lin A, McMahon M, Lange-Carter, C, Derifard B, Davis R, Johnson G, and Karin M. Bifurcation in Ras signaling: Raf-1 and MEKK-1 differentially activate ERK and JNK MAP kinases. Science. 256:1719-1723, 1994.
  4. Lin A, Minden A, Martinetto H, Claret FX, Lange-Carter C, Mercurio F, Johnson GL, and Karin M. Identification of a dual specificity kinase that activates the Jun kinases and p38-Mpk2. Science. 268:286-290, 1995.
  5. Minden A, Lin A, Claret FX, Abo A, and Karin M. Selective activation of the JNK signaling cascade and c-Jun transcriptional activity by the small GTPases Rac and Cde42Hs. Cell. 81:1147-1157, 1995.
  6. Lu X, Nemoto S, and Lin A*. Identification of c-Jun NH2-terminal protein kinase (JNK)-activating kinase 2 as an activator of JNK but not p38. Journal of Biological Chemistry (Communication). 272:24751-24754, 1997.
  7. Nemoto S, DiDonato J A, and Lin A*. Coordinate regulation of IkB kinase by MEKK1 and NIK. Molecular and Cellular Biology . 18:7336-7343, 1998.
  8. Zheng C, Xiang J, Hunter T, and Lin A*. Generation of a constitutively active c-Jun N-terminal protein kinase that stimulates c-Jun transcription activity. Journal of Biological Chemistry. 274:28966-28971, 1999.
  9. Purcell NH, Tang G, Yu C, Mercurio F, DiDonato JA, and Lin A*. Activation of NF-kB is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes. Proceedings of the National Academy of Science USA. 98:6668-6673, 2001.
  10. Tang G, Yang J, Minemoto Y, and Lin A*. Blocking caspase-3-mediated proteolysis of IKKb suppresses TNF-a-induced apoptosis. Molecular Cell. 8:1005-1016, 2001.
  11. Tang G, Minemoto Y, Dibling B, Purcell NH, Li Z, Karin M, and Lin A*. Inhibition of JNK activation by NF-kB target genes. Nature. 414:313-317, 2001. - News and Views, Nature. 414:265-266, 2001; Highlights, Nature Reviews, 2: 875, 2001; Hot Papers, The Scientist, 12:32-33, 2003.
  12. Tang F, Tang G, Xiang J, Dai Q, Rosner MR, and Lin A*. Absence of NF-kB-mediated inhibition of JNK activation contributes to TNF-a induced apoptosis in MCF-7 cells. Molecular and Cellular Biology. 22:8571-8579, 2002.
  13. Karin M and Lin A. NF-kB at the crossroad of life and death. Nature Immunology. 3:221-227, 2002. - One of the most cited papers in the field, ISI.
  14. Lin A* and Dibling B. The true face of JNK activation in apoptosis. Aging Cell. 1:112-116, 2002.
  15. Lin A. Activation of the JNK signaling pathway: Breaking the Brake on Apoptosis. BioEssays. 25:17-24, 2003.
  16. Lin A*and Karin M. NF-kB in cancer: A marked target. Seminars in Cancer Biology. 13:107-114, 2003.
  17. Yu C, Minemoto Y, Zhang J, Liu J, Tang F, Bui T, Xiang J*, and Lin A*. JNK suppresses apoptosis via phosphorylation of the proapoptotic Bcl-2 family protein BAD. Molecular Cell. 13:329-40, 2004.
  18. Liu J, Minemoto Y, and Lin A*. JNK1, but not JNK2, is essential for TNF-a-induced c-Jun kinase activation and apoptosis. Molecular and Cellular Biology. 24:10844-10856, 2004.
  19. Lin A. The role of JNK in apoptosis: A double-edged sword. In Anning Lin eds., The JNK signaling pathway. TX: Landers Bioscience. 63-69, 2006.
  20. Liu J, Yang D, Minemoto Y, Leitges M, Rosner M.R and Lin A*. NF-kB via PKCd promotes JNK activation by UV. Molecular Cell. 21:467-480, 2006.
  21. Lin, A. A Five-Year Itch for TNF-a Cytotoxicity: The Time Factor Determines JNK Action. Development Cell. 10:277-278, 2006.
  22. Liu J, and Lin A*. The NF-kB and JNK1 crosstalk: wiring the cell signaling circuitry in human diseases. Oncogene, 3267-3278, 2007.
  23. Liu J, Zhao Y, Eilers M, and Lin A*. Miz1 is a signal- and pathway-specific modulator or regulator (SMOR) that suppresses TNF-a-induced JNK1 activation. Proceedings of the National Academy of Science USA. 106(43):18279-84, 2009.
  24. Lin A*. ATIA: A Link between Inflammation and Hypoxia. Molecular Cell 42: 557-558, 2011.
  25. Liu J, Yan J, Jiang S, Wen J, Cheng L, Zhao Y, and Lin A*. Site-specific ubiquitination is required for relieving Miz1-mediated suppression on TNFα-induced JNK activation and inflammation. Proceedings of the National Academy of Science USA 109:191-6, 2012.
  26. Yan J, Xiang J, Lin Y, Ma J, Zhang J, Zhang H, Sun J, Danial N, Liu J, Lin A*. Inactivation of the BH3-only Protein BAD by IKK Inhibits TNFα-induced Apoptosis Independently of NF-κB Activation. Cell 152: 304-315, 2013.

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