程序性坏死参与了炎性疾病、癌症等病理过程，但其分子机制知之甚少。MLKL是 TNF诱导程序性坏死的执行蛋白，被RIPK3磷酸化后形成了二硫键依赖的类淀粉样多聚体而诱导坏死。本实验室主要调查MLKL多聚体诱导程序性坏死的分子机制，以及炎性疾病和癌症中的程序性坏死机制，以期找到治疗此类疾病的治疗靶点。

教育经历

山西大学：学士

中国科学院微生物研究所：硕士

德国罗斯托克大学：博士

工作经历

中国科学院过程工程研究所：研实员

美国德克萨斯大学西南医学中心：博士后、助理讲师、讲师

安徽医科大学：校聘教授、博导、博士后合作导师

欢迎有志从事细胞死亡、炎症及肿瘤研究工作的青年（硕士、博士及博士后）加入我们团队。

博士后招聘常年有效，具体待遇及更新参见人事处相关网页。

1. 国家自然科学基金面上项目一项，主持；

2. 安徽医科大学引进人才科研启动项目，主持。

1. Liu, S. Z., Perez P., Sun X., Fatirkhorani R., Mammadova J., Chen K., Wang, Z. G.. MLKL polymerization-induced lysosomal membrane permeabilization promotes necroptosis. Cell Death & Differentiation, 2023, 31 (1), 40-52.

2. Deng, H.S., Guo, X.L., Feng, N., Luo, Y., Liu, B., Liu, S. Z.*, Wu, J.I. *, Shi, X.M.. * Targeting H3K27me3 demethylase to inhibit Shh signaling and cholesterol metabolism in medulloblastoma growth. Frontiers in Oncology, 2022, 12, 1057147 (*co-corresponding author).

3. Du,J.C., Xiang, Y.G., Liu, H., Liu, S. Z., Kumar, A., Xing, C., Wang, Z. G.. PPP1R3G/PP1γ is essential for RIPK1 dephosphorylation and RIPK1 kinase activation to promote apoptosis and necroptosis in vitro and in vivo. Nature Communications, 2021, 12 (1), 7067.

4. Bersch, K., DeMeester, K., Zagani, R., Chen, S.Y., Wodzanowski, K., Liu, S. Z., Mashayekh, S., Reinecker, H.C, Grimes, C.. Bacterial Peptidoglycan Fragments Differentially Regulate Innate Immune Signaling. ACS Central Science. 2021, 7(4): 688-696. 

5. Johnston, A.N., Ma, Y.Y., Liu, H., Liu, S. Z., Addams, S.-H., Chen, S., Chen, C., Wang, Z. G.. Novel necroptosis-blocking compound NBC1 targets heat shock protein 70 to inhibit MLKL Polymerization and necroptosis. Proc Natl Acad Sci U S A. 2020, 117(12):6521-6530. 

6. Addams, S.-H., Liu, S. Z., Liu, H., Wang, Z. G.. CK1a, CK1d and CK1e are necrosome components which phosphorylate serine 227 of human RIPK3 to activate necroptosis. Proc Natl Acad Sci U S A. 2020,117(4):1962-1970. 

7. Liu, S. Z., Liu, H., Johnston, A., Addams, S.-H., Reynoso, E., Xiang, Y.G., Wang, Z. G.. MLKL forms disulfide bond-dependent amyloid-[like] polymers to induce necroptosis. Proc Natl Acad Sci U S A. 2017,114(36):E7450-E7459. 

8. Hu, M.C., Shi, M., Cho, H.J., Zhang, J., Pavlenco, A., Liu, S. Z., Sidhu, S., Huang, L.J, Moe, O.W..The erythropoietin receptor is a downstream effector of Klotho-induced cytoprotection. Kidney Int. 2013,84(3):468-81. 

9. Liu, S. Z., Shi, X. M., Bauer, I., Guenther, J., & Seyfert, H.-M.. Lingual Antimicrobial Peptide and IL-8 expression are oppositely regulated by the antagonistic effects of NF-kB p65 and C/EBPb in mammary epithelial cells. Mol. Immunol. 2011,48(67):895-908. 

10. Rebl, A., Rebl, H., Liu, S. Z., Goldammer, T., Seyfert, H.-M.. Salmonid Tollip and MyD88 factors can functionally replace their mammalian orthologues in TLR mediated trout SAA promoter activation. Dev. Comp. Immunol. 2011,35(1):81-7. 

11. Shi, X. M. ^#, Liu, S. Z.^#, Metges, C.C., and Seyfert, H.-M.. C/EBP-beta drives expression of the nutritionally regulated promoter IA of the acetyl-CoA carboxylase alpha gene in cattle. Biochim. Biophys. Acta-gene regulatory mechanisms 2010,1799(8):561-7. (#: co-first author).

12. Guenther, J., Liu, S. Z., Esch, K., Schuberth, H.-J., Seyfert, H.-M.. Stimulated expression of TNF-alpha and IL-8, but not of lingual antimicrobial peptide reflects the concentration of pathogens contacting bovine mammary epithelial cells. Vet. Immunol. Immunop. 2010,135(1-2):152-7.

13. Liu, S. Z., & Qian, S. J.. Purification and properties of laccase from Wei Sheng Wu Xue Bao (in Chinese), 2003,43,73-78.

14. Liu, W. X., Chao, Y. P., Liu, S. Z., Bao, H. B., & Qian, S. J. (2003). Molecular cloning and characterization of a laccase gene from the basidiomycete Fome lignosus and expression in Pichia pastoris. Applied Microbiology and Biotechnology, 2003,63,174-181.