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. 2018 Jul 18;6:21. doi: 10.1038/s41413-018-0022-y

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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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Fig. 7 — PTH stimulates transport of PTH1R to primary cilia of NP cells. a Immunostaining for acetylated α-tubulin (green) and DAPI (blue) showing the length of primary cilia of NP cells from PTH1R-deficient mice or PTH1R^+/+ mice. b Quantitative measurements of primary cilia length of (a). c Immunostaining for acetylated α-tubulin or PTH1R showing that PTH-stimulated transport of PTH1R to primary cilia of NP cells. d Quantitative analysis of PTH1R intensity in cilia of (c). e Immunostaining for DAPI, pCREB, or acetylated α-tubulin showing that PTH-stimulated phosphorylation of CREB at primary cilia of NP cells. f Quantitative analysis of pCREB intensity in cilia of (e). g, h Co-immunoprecipitation of cell lysates from NP cells treated with PTH or vehicle using antibody against pCREB and blotted with PTH1R (g) or using antibody against PTH1R and blotted with pCREB (h) showing the interaction between PTH1R and pCREB in the acetylated α-tubulin extracts. *P < 0.05. n = 8 per group. Statistical significance was determined by one-way ANOVA and Student's t-test. All data are reported as the mean ± s.d.