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. 2020 Apr 13;78(1):351–372. doi: 10.1007/s00018-020-03510-1

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© The Author(s) 2020

Open AccessThis 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/.

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Fig. 10 — Model of the Impact of the CMT2B-causing RAB7 mutant protein on the endocytic pathway. In CMT2B the presence of RAB7^V162M causes an increase of late endosomal proteins and enzymes as well as of lysosomal activity. This, in turn, activates a feedback control mechanism demonstrated by the decrease of ESCRT proteins. Because of the presence of the RAB7 mutant, CMT2B cells fail to respond to this regulatory mechanism, showing higher lysosomal activity