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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Mol Cancer Res. 2017 Sep 28;16(1):58–68. doi: 10.1158/1541-7786.MCR-17-0408

Figure 5. JG-98 Activity Occurs through a RIP1-Dependent Process.

Figure 5

(A) RIP1 KO Jurkat cells are resistant to JG-98. Viability was determined by trypan blue exclusion. Cells were treated for 24 hrs with JG-98 (10 μM), 17-DMAG (10 μM), bortezomib (40 nM), etoposide (20 μM). Results are the average of three independent experiments performed in triplicate. ns = not significant; * p < 0.05. (B) JG-98 activity requires RIP1 kinase. MDA-MB-231 cells were pretreated with 20 μM necrostatin-1 for 1 hour prior to addition of compounds. Viability was determined by three independent MTT assays performed in quintuplicate. Error is SEM. ns = not significant; ***p < 0.0001. (C) JG-98 induces degradation of RIP1 modulators. MDA-MB-231 cells were treated for 24 hours. Results represent experiments performed in triplicate. (D) RIP1 regulators are rapidly degraded in response to JG-98. MDA-MB-231 cells were treated with JG-98 (10 μM). Results are representative of duplicates.