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. 2022 Jun 27;13:922825. doi: 10.3389/fendo.2022.922825

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Copyright © 2022 Pablos, Casanueva-Álvarez, González-Casimiro, Merino, Perdomo and Cózar-Castellano

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Non-proteolytic functions of IDE in α-cells. (A) The abundance of IDE in pancreatic α-cells is relevant for maintaining several cellular functions, such as glucagon secretion, cytoskeletal organization, and ciliogenesis, while cells are maintained in a quiescent state. (B) Deletion of IDE in mouse α-cells revealed multiple phenotypes, such as hyperglucagonemia, hyperplasia, and hypertrophy, suggesting different non-proteolytic functions of IDE in these cells. Lack of primary cilia along with increased proliferation, in Ide depleted α-cells, provide direct functional evidence for the involvement of cilia in α-cell proliferation. Likewise, loss of IDE causes α-synuclein aggregation, which might underlie the absence of cilia, cytoskeletal alterations, and augmented SNARE proteins of the secretory machinery. This figure was created using Servier Medical Art (available at https://smart.servier.com/).