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. 2019 Jul 30;9:11057. doi: 10.1038/s41598-019-46677-9

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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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Endogenous Calmodulin and Cdc42, but not Endogenous Ras, Associate with Endogenous IQGAP3 and IQGAP1. Endogenous IQGAP1 (IQ1) (panels A, B and C) or IQGAP3 (IQ3) (panels D, E and F) was immunoprecipitated (IP) from untransfected HEK293 cell lysates. Non-immune rabbit serum (NIRS) was used as a negative control. Precipitates and 1% of the lysate (1% input) used for each experiment were resolved by SDS-PAGE and analyzed by Western blotting. Blots were probed for IQGAP1 (panels A, B and C) or IQGAP3 (panels D, E and F) and calmodulin (panels A, D), Cdc42 (panels B,E), or Ras (panels C, F). Ras was detected using a pan Ras antibody that recognizes the isoforms H-,K-, and N-Ras. Numbers indicate the positions of migration of molecular weight markers. Each panel depicts two sections from a single blot (i.e. three blots in total for IQGAP1 and three for IQGAP3). Blots were cropped for clarity. The full-length blots can be found in Supplementary Fig. 5. Data shown are representative of at least two independent experiments.