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. 2024 May 23;57:31. doi: 10.1186/s40659-024-00501-5

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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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Elimination of the R33-E162 interaction in the intracellular pocket impairs gap junctional plaque formation. Photomicrographs show the distribution of immunoreactive Cx50, Cx50R33E, Cx50E162R and Cx50R33E,E162R in transfected HeLa cells. Gap junctional plaques formed by Cx50 and the double mutant, Cx50R33E,E162R, are indicated by arrows. Scale bar, 20 μm