Revising endosomal trafficking under insulin receptor activation
Keywords: 
Insulin receptor
Endocytosis
Receptor trafficking
Endosomal recycling compartment
Arf GTPases
Ras GTPases
Issue Date: 
2021
ISSN: 
1422-0067
Note: 
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license
Citation: 
Iraburu-Elizalde, M. (María José); Garner, T.; Montiel-Duarte, C.. "Revising endosomal trafficking under insulin receptor activation". International Journal of Molecular Sciences. 22 (13), 2021, 6978
Abstract
The endocytosis of ligand-bound receptors and their eventual recycling to the plasma membrane (PM) are processes that have an influence on signalling activity and therefore on many cell functions, including migration and proliferation. Like other tyrosine kinase receptors (TKR), the insulin receptor (INSR) has been shown to be endocytosed by clathrin-dependent and -independent mechanisms. Once at the early endosome (EE), the sorting of the receptor, either to the late endosome (LE) for degradation or back to the PM through slow or fast recycling pathways, will determine the intensity and duration of insulin effects. Both the endocytic and the endosomic pathways are regulated by many proteins, the Arf and Rab families of small GTPases being some of the most relevant. Here, we argue for a specific role for the slow recycling route, whilst we review the main molecular mechanisms involved in INSR endocytosis, sorting and recycling, as well as their possible role in cell functions.

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