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. 2019 Sep 16;9:13342. doi: 10.1038/s41598-019-49646-4

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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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VEGFR2 colocalizes with RAB13 on filopodia in TBC1D10A/C expressing cells after VEGF-A165a stimulation. (A) PAE cells stably expressing VEGFR2 and NRP1 were transiently transfected with TBC1D10A and Cherry-RAB13. Cells were fixed 30 minutes after stimulation with VEGF-A165a and immunostained for VEGFR2. VEGFR2 and RAB13 colocalize with TBC1D10A on filopodia (arrows). (B) Transient transfection of TBC1D10B and Cherry-RAB13. TBC1D10B positive filopodia are negative for VEGFR2 (arrowheads). TBC1D10B and RAB13 colocalize at the plasma membrane. (C) In TBC1D10C and RAB13 expressing cells, TBC1D10C, RAB13, and VEGFR2 colocalize on filopodia (arrows). (D) Coexpression of TBC1D10B with a constitutive active form of RAB13. Expression of RAB13-Q67L induces filopodia in unstimulated cells that are negative for VEGFR2 (arrowheads). (E) Thirty minutes after stimulation with VEGF A165a, filopodia contain VEGFR2. Scale bar: 10 µm.