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. Author manuscript; available in PMC: 2022 Aug 1.
Published in final edited form as: Mol Cancer Res. 2021 Oct 15;20(2):231–243. doi: 10.1158/1541-7786.MCR-20-1076

Figure 7. Model of SGK2-, 14-3-3-, and HUWE1-mediated regulation of PTOV1 localization, stability, and function.

Figure 7.

Our data suggest that an SGK2-governed interaction between 14-3-3 and PTOV1 sequesters PTOV1 in the cytosol, which promotes PTOV1-mediated expression of cJun. Upon loss of 14-3-3 binding, PTOV1 accumulates in the nucleus and is subject to HUWE1-dependent degradation via the proteasome.