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. 2014 Aug 13;3(5):1211–1224. doi: 10.1002/cam4.298

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© 2014 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fbw7 possibly governs Klf4 stability in a GSK3-dependent manner. (A) Fbw7-siRNA treatment in HeLa cells led to increased Klf4 expression. (B) Fbw7-shRNA treatments in HeLa cells led to Klf4 accumulation. (C) Overexpression of Fbw7 and GSK3 led to the destruction of Klf4. 293T cells were cotransfected with HA-Fbw7, Flag-Klf4 and indicated kinases and Klf4 abundance was measured by immunoblots with anti-Flag antibody. GFP was included as an internal transfection control and tubulin served as a loading control. (D) GSK3β-shRNA treatments in HeLa cells led to elevated level of Klf4. (E and F) Sequence alignment of the putative Fbw7 degrons in Klf4 (E) among different species (F).