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. 2018 Mar 12;8:4378. doi: 10.1038/s41598-018-21031-7

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© The Author(s) 2018

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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Homodimeric INSR controls IGF-1R expression. (A) hTCEpi cells treated with siRNA oligonucleotides targeting the INSR resulted in a small increase in IGF-1R in growth media. (B) In contrast, siRNA knockdown of INSR in basal media induced a large increase in IGF-1R expression compared to the non-targeting control. Immunoblotting for INSR confirmed knockdown of the INSR. GAPDH was used as a loading control. (C) Similarly, siRNA knockdown of IGF-1R in growth media led to a small increase in INSR in growth media. (D) However, siRNA knockdown of IGF-1R in basal media led to a major reduction in INSR levels. Immunoblotting for IGF-1R confirmed knockdown of the receptor. β-actin was used as a loading control.