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. 2021 Feb 15;18(1):105–119. doi: 10.20892/j.issn.2095-3941.2020.0098

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Copyright: © 2021, Cancer Biology & Medicine

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY) 4.0, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

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HBXIP prevents proteasome-mediated MEK1 degradation. (A) MEK1 protein stability in HBXIP-deficient A549 and H1299 cells was assessed by Western blot (left panel), and protein levels were quantified (right panel) after cells were treated with cycloheximide for 2 or 4 h. (B) Western blot of MEK1 protein in HBXIP knockdown A549 and H1299 cells treated with MG132 for 2 and 4 h. (C) Immunofluorescence staining of HBXIP and MEK1 in HBXIP-overexpressing A549 cells and the quantified staining intensity of HBXIP and MEK1 (lower panel). Scale bars, 50 μm. (D) Immunoprecipitation of MEK1 by anti-FLAG beads in cell extracts of A549 cells overexpressing FLAG-tagged HBXIP. The results were analyzed by an unpaired t-test. **P < 0.01; ***P < 0.001.