Pascual-Caro C, Espinosa-Bermejo N, Pozo-Guisado E, Martin-Romero FJ. Role of STIM1 in neurodegeneration. World J Biol Chem 2018; 9(2): 16-24 [PMID: 30568747 DOI: 10.4331/wjbc.v9.i2.16]
Corresponding Author of This Article
Francisco Javier Martin-Romero, PhD, Associate Professor, Department of Biochemistry and Molecular Biology, School of Life Sciences and Institute of Molecular Pathology Biomarkers, University of Extremadura, Avenida de Elvas s/n, Badajoz 06006, Spain. fjmartin@unex.es
Research Domain of This Article
Biochemistry & Molecular Biology
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Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Biol Chem. Nov 16, 2018; 9(2): 16-24 Published online Nov 16, 2018. doi: 10.4331/wjbc.v9.i2.16
Role of STIM1 in neurodegeneration
Carlos Pascual-Caro, Noelia Espinosa-Bermejo, Eulalia Pozo-Guisado, Francisco Javier Martin-Romero
Carlos Pascual-Caro, Noelia Espinosa-Bermejo, Francisco Javier Martin-Romero, Department of Biochemistry and Molecular Biology, School of Life Sciences and Institute of Molecular Pathology Biomarkers, University of Extremadura, Badajoz 06006, Spain
Eulalia Pozo-Guisado, Department of Cell Biology, School of Medicine and Institute of Molecular Pathology Biomarkers, University of Extremadura, Badajoz 06006, Spain
Supported bythe Spanish Ministerio de Ciencia, Innovación y Universidades, No. BFU2017-82716-P.
Author contributions: Martin-Romero FJ wrote the initial draft; Pascual-Caro C, Espinosa-Bermejo N and Pozo-Guisado E revised and reformatted the final version of the manuscript, together with Martin-Romero FJ; all authors approved the version to be published.
Conflict-of-interest statement: The authors declare that they have no conflict of interests.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Francisco Javier Martin-Romero, PhD, Associate Professor, Department of Biochemistry and Molecular Biology, School of Life Sciences and Institute of Molecular Pathology Biomarkers, University of Extremadura, Avenida de Elvas s/n, Badajoz 06006, Spain. fjmartin@unex.es
Telephone: +34-92-4489971
Received: August 15, 2018 Peer-review started: August 17, 2018 First decision: September 11, 2018 Revised: October 8, 2018 Accepted: October 23, 2018 Article in press: October 23, 2018 Published online: November 16, 2018
Abstract
STIM1 is an endoplasmic reticulum (ER) protein with a key role in Ca2+ mobilization. Due to its ability to act as an ER-intraluminal Ca2+ sensor, it regulates store-operated Ca2+ entry (SOCE), which is a Ca2+ influx pathway involved in a wide variety of signalling pathways in eukaryotic cells. Despite its important role in Ca2+ transport, current knowledge about the role of STIM1 in neurons is much more limited. Growing evidence supports a role for STIM1 and SOCE in the preservation of dendritic spines required for long-term potentiation and the formation of memory. In this regard, recent studies have demonstrated that the loss of STIM1, which impairs Ca2+ mobilization in neurons, risks cell viability and could be the cause of neurodegenerative diseases. The role of STIM1 in neurodegeneration and the molecular basis of cell death triggered by low levels of STIM1 are discussed in this review.
Core tip: STIM1 is an endoplasmic reticulum protein that regulates store-operated Ca2+ entry, which is a Ca2+ influx pathway involved in a wide variety of signalling pathways. Growing evidence supports a role for this protein, STIM1, in long-term potentiation and the formation of memory. In this regard, the loss of STIM1 observed in brain tissue from Alzheimer’s disease patients risks cell viability and could be the cause of neurodegenerative diseases. This is the reason for discussing the role of STIM1 in neurodegeneration in this review.
