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. 2024 Sep 6;15(9):655. doi: 10.1038/s41419-024-07013-w

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Ishikawa cell lysates were incubated with an anti-RAF17 antibody, and interacting proteins were detected by Western blot analysis with an anti-TFRC antibody. B Ishikawa cell lysates were incubated with an anti-TFRC antibody, and interacting proteins were detected by Western blot analysis with an anti-RAB17 antibody. C Ishikawa and HEC-1A cells were infected with Lv-NC and Lv-RAB17. CHX (20 μmol) was added for the indicated time, and the cell lysates were subjected to Western blot analysis for RAB17 and TFRC. D Ishikawa and HEC-1A cells were transfected with NC-si or RAB17-si1. CHX (20 μmol) was added for the indicated time, and the cell lysates were subjected to Western blot analysis for RAB17 and TFRC. E Ishikawa and HEC-1A cells were infected with Lv-NC and Lv-RAB17. The cells were then treated with the MG132 proteasome inhibitor (20 mmol) for 12 h, and Western blot analysis was performed with anti-RAB17 and anti-TFRC antibodies. F Ishikawa and HEC-1A cells were transfected with Lv-NC or Lv-RAB17. The cells were then treated with the lactacystin proteasome inhibitor (10 mmol) for 12 h, and Western blot analysis was performed with anti-RAB17 and anti-TFRC antibodies. G Ishikawa and HEC-1A cells were transfected with NC-si or RAB17-si1. The cells were then transfected with His-tagged ubiquitin-containing vectors (His-Ub) for 12 h, and Western blot analysis was performed with anti-RAB17 and anti-TFRC antibodies. H Ishikawa and HEC-1A cells were transfected with NC-si or RAB17-si1. The cells were then treated with the chloroquine lysosomal inhibitor (10 mmol) for 12 h, and Western blot analysis was performed with anti-RAB17 and anti-TFRC antibodies. I, J Ishikawa and HEC-1A cells were transfected as indicated and treated with MG132 for 12 h. Lysates were immunoprecipitated with anti-TFRC and detected with anti-His. GAPDH was used as an internal control. K Ishikawa cells were infected with Lv-CTL or Lv-RAB17, and cell lysates were immunoprecipitated with the indicated primary antibody and immunoblotted as indicated. L, M Ishikawa cells were transfected as indicated, and then cell lysates were immunoprecipitated with anti-TFRC antibody and detected with anti-His antibody. All the above assays were independently performed in triplicate (N = 3). ***P < 0.001.