Participating Faculty

Weihang Chai

Weihang Chai

Department:School of Molecular Biosciences/Medical Sciences
Credentials:1999 - Ph.D., Cornell University
Office:WSU Spokane
Mailing Address:

Medical Sciences
PO Box 1495
Spokane, WA 99210-1495
Website:Click here

Research Interests

Mechanisms governing genome stability

Research Summary

The overall goal of research in my lab is to understand the mechanisms governing genome stability, and more importantly, how we can apply new knowledge to prevent genome instability as well as to fight against cancer and aging-related diseases. We are carrying out three areas of research in parallel: a) maintenance of the stability of fragile sites in the genome in response to environmental genotoxins, b) maintenance of telomere integrity, and c) translational research. We apply innovative approaches including next-generation sequencing, advanced fluorescent microscopy, and genome editing to accomplish our research goals. 

Research Publications

Huang, C., Jia, P., Chastain, M., Shiva, O., Dai, X., *Chai, W. (2017) The Human CTC1/STN1/TEN1 Complex Localizes in ALT-Associated PML Bodies and Regulates Telomere maintenance in ALT cancer cells. Exp Cell Res. 355(2):95-104.                           

Jia, P., Chastain, M., Zou, Y., Her, C., *Chai, W. (2017) Human MLH1 suppresses the insertion of telomeric sequences at intra-chromosomal sites in telomerase-expressing cells. Nucleic Acids Res. 45(3):1219-1232.                                               

Chastain, M., Zhou, Q., Shiva, O., Fadri-Moskwik, M., Whitmore, L., Jia, P., Dai, X., Huang, C., Ye, P., *Chai, W. (2016) Human CST facilitates genome-wide RAD51 recruitment to GC-rich repetitive sequences in response to replication stress.  Cell Reports. 16(5):1300-14                                                                

Zhou, Q.V., Sampathi, S., *Chai, W.  (2016)   Suppression of STN1 Enhances the Cytotoxicity of Chemotherapeutic Agents in Cancer Cell Lines by Increasing DNA Damages. Oncology Letters. 12(2):800-808                                                       

Chung, L., et al. (2015). "The FEN1 E359K germline mutation disrupts the FEN1-WRN interaction and FEN1 GEN activity, causing aneuploidy-associated cancers." Oncogene 34(7): 902-911.                                                                                   

Jia, P., Her, C., *Chai, W.   (2015)  DNA Excision Repair at Telomeres. DNA Repair. 36:137-45.                              

Chung, L., Onyango, D., Guo, Z., Jia, P., Dai, H., Lin, W., Pang, I., Li, H., Yuan, Y., Huang, Q., Zheng, L., Lopes, J., Nicolas, A., Chai, W., Raz, D., Reckamp, K.L., Shen, B.   (2015)   The FEN1 E359K mutation isolated from a breast cancer patient disrupts the FEN1-WRN interaction and FEN1 GEN activity, causing aneuploidy-associated cancers. Oncogene. 34(7):902-11.   PMID: 24608430


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