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. Author manuscript; available in PMC: 2017 Jul 16.
Published in final edited form as: Cancer Lett. 2017 Jan 13;390:11–20. doi: 10.1016/j.canlet.2017.01.003

Fig. 5. SPOP mutants are impaired to interact with and degrade EglN2.

Fig. 5

(A) A schematic illustration of SPOP domains and prostate cancer-associated mutations. (B) IB analysis of WCLs and IPs derived from 293T cells transfected with the indicated plasmids. The resulting cells were treated with MG132 (10 μM) for 10 h before harvesting. (C) In vitro GST pull-down assay demonstrated SPOP mutations impaired to interact with EglN2. (D) IB analysis of WCLs derived from 293T cells transfected with the indicated constructs. (E) IB analysis of LNCaP cells stably infected with indicated constructs. (F) IB analysis of WCLs and His pull-down products derived from 293T cells transfected with constructs encoding indicated proteins and treated with MG132 (10 μM) for 10 h before harvesting. (G) Schematic diagrams illustrate how SPOP regulates EglN2. Specifically, WT-SPOP could interact with and degrade EglN2, while loss-of-function mutations SPOP impaired its capability to destruct EglN2, importantly, SPOP could not recognize and destruct degrons deletion form of EglN2.