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. 2019 Feb 25;9:2724. doi: 10.1038/s41598-019-39368-y

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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FBXO38 interacts with and stabilizes KIF20B by an SCF-independent mechanism. (A) AGS cells were cotransfected with plasmids expressing HA-tagged KIF20B and FLAG-tagged FBXO38 (WT), the FBXO38 F-box deletion mutant (∆FBX) or an empty vector control (VC). Cell lysates were analyzed by Western blotting using antibodies against FLAG and HA. (B) 293 T cells were cotransfected as in (A), followed by coimmunoprecipitation using anti-FLAG M2 resin. Recovered proteins were analyzed by Western blotting using antibodies against FLAG, HA and Skp1 and myc. Bands corresponding to FBXO38 WT or ∆FBX are indicated with arrow heads. (C) AGS cells were transfected with an siRNA targeting FBXO38 (+) or a negative control siRNA (−) followed by 12 hr treatment with the MG132 proteasome inhibitor (+) or DMSO (−). Cell lysates were analyzed by Western blotting using antibodies against FBXO38, KIF20B and actin.