Supplementary Information
A Gemcitabine Sensitivity Screen Identifies a Role for NEK9 in the Replication Stress Response Scott C. Smith1, Aleksandra V. Petrova1, Matthew Z. Madden1, Hongyan Wang1, Yunfeng Pan1, Matthew D. Warren1, Claire W. Hardy1, Dong Liang1, Elaine A. Liu1, M. Hope Robinson1, Soumon Rudra1, Jie Wang1, Shahrzad Ehdaivand2, Mylin A. Torres1, Ya Wang1, and David S. Yu1,* 1
Department of Radiation Oncology, Emory University School of Medicine, Atlanta, GA 30322 USA 2 Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322 USA * Corresponding Author: David S. Yu, M.D., Ph.D. Department of Radiation Oncology Emory University School of Medicine 1365 Clifton Rd NE, C3008 Phone: 404-778-1758, Fax: 404-778-5520 e-mail:
[email protected] Inventory of Supplementary Information Figure S1 Figure S2 Figure S3 Figure S4 Table S1 Table S2 Table S3
Supplementary Figure S1. Synthetic lethal screen controls. Western blot analysis demonstrating efficiency of ATR and CHK1 knockdown with indicated siRNAs in MDA-MB231 cells.
Supplementary Figure S2. NEK9 depletion causes replication stress hypersensitivity. (A) MIA PaCa-2 cells were transfected with NT, ATR, or NEK9 siRNA, split 1:4 24 hours later, and treated 24 hours later with or without 5 uM gemcitabine for 72 hours prior to assaying for cell viability. Mean and standard deviation of gemcitabine treated to untreated cell viability relative to NT siRNA from three replicas is shown. * p
