林安宁

个人简介：

林安宁教授1990年在美国阿拉巴马州立大学伯明翰分校(UAB)获博士学位。1991年在美国加州大学圣地亚哥分校(UCSD)从事博士后研究。1996年在美国阿拉巴马州立大学伯明翰分校任准聘助理教授。1999年在美国芝加哥大学任准聘助理教授，2002年晋升为终身副教授，2006年晋升为终身正教授。2009年回国任中科院上海生化与细胞所所长，课题组长，博士生导师，终身正教授, 国家特聘教授。2014年回美国芝加哥大学任终身正教授。2020年回国任南京大学现代生物研究院创院院长，独立学科带头人（Principal Investigator, PI），博士生导师，终身正教授，国家特聘教授，南京大学医学院附属鼓楼医院特聘教授。2021年入选江苏省“双创人才”，2022年入选南京市“A类”人才（唯一入选者）。

林安宁教授是JNK-c-Jun 信号转导通路的主要发现者之一，在Cell， Nature、Science， Molecular Cell、PNAS等著名国际期刊发表80余篇研究论文，论文总引用数超过20,000次。林安宁教授长期以来研究细胞信号转导网络的分子机理及其调控异常在疾病中的作用，其在美国的研究工作长期受到NIH经费支持。在2009到2014年期间，林安宁教授曾担任科技部重大研究计划项目首席科学家，其研究工作也得到基金委重点项目支持。目前担任Molecular and Cellular Biology和Cell Research编委。

研究方向：

1. 细胞信号转导网络异常与疾病 

2. 肿瘤免疫和自身免疫新机制

3. 生物人工智能

代表性论文：

Zhang, W., Zhangyuan, Y., Wang, F., Jin, K., Shen, H., Zhang, L., Yuan, X., Wang, J., Zhang, H., Yu, W., Huang, R., Xu, X., Yin, Y., Zhong, G., Lin, A*., Sun, B*. (2021). The zinc finger protein Miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation. Immunity. DOI: https://doi.org/10.1016/j.immuni.2021.04.027

Zhang, L., Qian, Y., Li, J., Zhou, X., Xu, H., Yan, J., Xiang, J., Yuan, X., Sun, B., Sisodia, S., Jiang, Y., Cao, X., Jing, N., Lin, A*. (2021). BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology. iScience. DOI: https://doi.org/10.1016/j.isci.2021.102942

Li, J., Zhang L., Zheng, Y., Shao, R., Liang, Q., Yu W., Wang, H., Zou, W., Wang, D., Xiang, J., Lin, A*. (2020). BAD inactivation exacerbates rheumatoid arthritis pathology by promoting survival of sublining macrophages. eLife 9: e56309.

Yan, J., Zhang, H., Xiang, J., Zhao, Y., Yuan, X., Sun, B., and Lin, A*. (2018). The BH3-only protein BAD mediates TNFalpha cytotoxicity despite concurrent activation of IKK and NF-kappaB in septic shock. Cell Res 28, 701-718.

Yan, J., Xiang, J., Lin, Y., Ma, J., Zhang, J., Zhang, H., Sun, J., Danial, N.N., Liu, J., and Lin, A*. (2013). Inactivation of BAD by IKK inhibits TNFalpha-induced apoptosis independently of NF-kappaB activation. Cell 152, 304-315.

Liu, J., Yan, J., Jiang, S., Wen, J., Chen, L., Zhao, Y., and Lin, A*. (2012). Site-specific ubiquitination is required for relieving the transcription factor Miz1-mediated suppression on TNF-alpha-induced JNK activation and inflammation. Proc Natl Acad Sci 109, 191-196.

Liu, J., Zhao, Y., Eilers, M., and Lin, A*. (2009). Miz1 is a signal- and pathway-specific modulator or regulator (SMOR) that suppresses TNF-alpha-induced JNK1 activation. Proc Natl Acad Sci 106, 18279-18284.

Liu, J., Yang, D., Minemoto, Y., Leitges, M., Rosner, M.R., and Lin, A*. (2006). NF-kappaB is required for UV-induced JNK activation via induction of PKCdelta. Mol Cell 21, 467-480.

Yu, C., Minemoto, Y., Zhang, J., Liu, J., Tang, F., Bui, T.N., Xiang, J., and Lin, A*. (2004). JNK suppresses apoptosis via phosphorylation of the proapoptotic Bcl-2 family protein BAD. Mol Cell 13, 329-340.

Tang, G., Minemoto, Y., Dibling, B., Purcell, N.H., Li, Z., Karin, M., and Lin, A*. (2001). Inhibition of JNK activation through NF-kappaB target genes. Nature 414, 313-317.

- (2001). News and Views, Nature 414, 265-266.

- (2001). Highlights, Nature Reviews 2, 875.

- (2003). Hot Papers, The Scientist 12,32-33.

Tang, G., Yang, J., Minemoto, Y., and Lin, A*. (2001). Blocking caspase-3-mediated proteolysis of IKKbeta suppresses TNF-alpha-induced apoptosis. Mol Cell 8, 1005-1016.

Purcell, N.H., Tang, G., Yu, C., Mercurio, F., DiDonato, J.A., and Lin, A*. (2001). Activation of NF-kappa B is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes. Proc Natl Acad Sci 98, 6668-6673.

Minden, A., Lin, A., Claret, F.X., Abo, A., and Karin, M. (1995). Selective activation of the JNK signaling cascade and c-Jun transcriptional activity by the small GTPases Rac and Cdc42Hs. Cell 81, 1147-1157.

Lin, A., Minden, A., Martinetto, H., Claret, F.X., Lange-Carter, C., Mercurio, F., Johnson, G.L., and Karin, M. (1995). Identification of a dual specificity kinase that activates the Jun kinases and p38-Mpk2. Science 268, 286-290.

Minden, A., Lin, A., McMahon, M., Lange-Carter, C., Derijard, B., Davis, R.J., Johnson, G.L., and Karin, M. (1994). Differential activation of ERK and JNK mitogen-activated protein kinases by Raf-1 and MEKK. Science 266, 1719-1723.

Hibi, M., Lin, A., Smeal, T., Minden, A., and Karin, M. (1993). Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. Genes Dev 7, 2135-2148.

Lin, A., Frost, J., Deng, T., Smeal, T., al-Alawi, N., Kikkawa, U., Hunter, T., Brenner, D., and Karin, M. (1992). Casein kinase II is a negative regulator of c-Jun DNA binding and AP-1 activity. Cell 70, 777-789.

代表性综述：

Lin, A. (2011). ATIA: a link between inflammation and hypoxia. Mol Cell 42, 557-558.

Liu, J., and Lin, A. (2007). Wiring the cell signaling circuitry by the NF-kappa B and JNK1 crosstalk and its applications in human diseases. Oncogene 26, 3267-3278.

Lin, A. (2006). A five-year itch in TNF-alpha cytotoxicity: the time factor determines JNK action. Dev Cell 10, 277-278.

Lin, A. (2006). Regulation of apoptosis by the JNK signaling pathway. In Anning Lin eds., The JNK signaling pathway. TX: Landers Bioscience. 63-69.

Liu, J., and Lin, A. (2005). Role of JNK activation in apoptosis: a double-edged sword. Cell Res 15, 36-42.

Lin, A., and Karin, M. (2003). NF-kappaB in cancer: a marked target. Semin Cancer Biol 13, 107-114.

Lin, A. (2003). Activation of the JNK signaling pathway: breaking the brake on apoptosis. Bioessays 25, 17-24.

Karin, M., and Lin, A. (2002). NF-kappaB at the crossroads of life and death. Nat Immunol 3, 221-227.

- One of the most cited papers in the field (3,092 citations), ISI.