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The Function of KDEL Receptors as UPR Genes in Disease
The KDEL receptor retrieval pathway is essential for maintaining resident proteins in the endoplasmic reticulum (ER) lumen. ER resident proteins serve a variety of functions, including protein folding and maturation. Perturbations to the lumenal ER microenvironment, such as calcium depletion, can ca...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8196686/ https://www.ncbi.nlm.nih.gov/pubmed/34063979 http://dx.doi.org/10.3390/ijms22115436 |
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author | Wires, Emily S. Trychta, Kathleen A. Kennedy, Lacey M. Harvey, Brandon K. |
author_facet | Wires, Emily S. Trychta, Kathleen A. Kennedy, Lacey M. Harvey, Brandon K. |
author_sort | Wires, Emily S. |
collection | PubMed |
description | The KDEL receptor retrieval pathway is essential for maintaining resident proteins in the endoplasmic reticulum (ER) lumen. ER resident proteins serve a variety of functions, including protein folding and maturation. Perturbations to the lumenal ER microenvironment, such as calcium depletion, can cause protein misfolding and activation of the unfolded protein response (UPR). Additionally, ER resident proteins are secreted from the cell by overwhelming the KDEL receptor retrieval pathway. Recent data show that KDEL receptors are also activated during the UPR through the IRE1/XBP1 signaling pathway as an adaptive response to cellular stress set forth to reduce the loss of ER resident proteins. This review will discuss the emerging connection between UPR activation and KDEL receptors as it pertains to ER proteostasis and disease states. |
format | Online Article Text |
id | pubmed-8196686 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-81966862021-06-13 The Function of KDEL Receptors as UPR Genes in Disease Wires, Emily S. Trychta, Kathleen A. Kennedy, Lacey M. Harvey, Brandon K. Int J Mol Sci Review The KDEL receptor retrieval pathway is essential for maintaining resident proteins in the endoplasmic reticulum (ER) lumen. ER resident proteins serve a variety of functions, including protein folding and maturation. Perturbations to the lumenal ER microenvironment, such as calcium depletion, can cause protein misfolding and activation of the unfolded protein response (UPR). Additionally, ER resident proteins are secreted from the cell by overwhelming the KDEL receptor retrieval pathway. Recent data show that KDEL receptors are also activated during the UPR through the IRE1/XBP1 signaling pathway as an adaptive response to cellular stress set forth to reduce the loss of ER resident proteins. This review will discuss the emerging connection between UPR activation and KDEL receptors as it pertains to ER proteostasis and disease states. MDPI 2021-05-21 /pmc/articles/PMC8196686/ /pubmed/34063979 http://dx.doi.org/10.3390/ijms22115436 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Wires, Emily S. Trychta, Kathleen A. Kennedy, Lacey M. Harvey, Brandon K. The Function of KDEL Receptors as UPR Genes in Disease |
title | The Function of KDEL Receptors as UPR Genes in Disease |
title_full | The Function of KDEL Receptors as UPR Genes in Disease |
title_fullStr | The Function of KDEL Receptors as UPR Genes in Disease |
title_full_unstemmed | The Function of KDEL Receptors as UPR Genes in Disease |
title_short | The Function of KDEL Receptors as UPR Genes in Disease |
title_sort | function of kdel receptors as upr genes in disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8196686/ https://www.ncbi.nlm.nih.gov/pubmed/34063979 http://dx.doi.org/10.3390/ijms22115436 |
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