Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer's Disease: Cell Cycle Reentry and Beyond

Inhibitor of DNA-binding/differentiation (Id) proteins, a family of helix-loop-helix (HLH) proteins that includes four members of Id1 to Id4 in mammalian cells, are critical for regulating cell growth, differentiation, senescence, cell cycle progression, and increasing angiogenesis and vasculogenesi...

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Veröffentlicht in:Cells (Basel, Switzerland) Switzerland), 2020-07, Vol.9 (7), p.1746, Article 1746
Hauptverfasser: Chen, Shang-Der, Yang, Jenq-Lin, Lin, Yi-Chun, Chao, A-Ching, Yang, Ding
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creator Chen, Shang-Der
Yang, Jenq-Lin
Lin, Yi-Chun
Chao, A-Ching
Yang, Ding
description Inhibitor of DNA-binding/differentiation (Id) proteins, a family of helix-loop-helix (HLH) proteins that includes four members of Id1 to Id4 in mammalian cells, are critical for regulating cell growth, differentiation, senescence, cell cycle progression, and increasing angiogenesis and vasculogenesis, as well as accelerating the ability of cell migration. Alzheimer's disease (AD), the most common neurodegenerative disease in the adult population, manifests the signs of cognitive decline, behavioral changes, and functional impairment. The underlying mechanisms for AD are not well-clarified yet, but the aggregation of amyloid-beta peptides (A beta s), the major components in the senile plaques observed in AD brains, contributes significantly to the disease progression. Emerging evidence reveals that aberrant cell cycle reentry may play a central role in A beta-induced neuronal demise. Recently, we have shown that several signaling mediators, including Id1, hypoxia-inducible factor-1 (HIF-1), cyclin-dependent kinases-5 (CDK5), and sonic hedgehog (Shh), may contribute to A beta-induced cell cycle reentry in postmitotic neurons; furthermore, Id1 and CDK5/p25 mutually antagonize the expression/activity of each other. Therefore, Id proteins may potentially have clinical applications in AD. In this review article, we introduce the underlying mechanisms for cell cycle dysregulation in AD and present some examples, including our own studies, to show different aspects of Id1 in terms of cell cycle reentry and other signaling that may be crucial to alter the neuronal fates in this devastating neurodegenerative disease. A thorough understanding of the underlying mechanisms may provide a rationale to make an earlier intervention before the occurrence of cell cycle reentry and subsequent apoptosis in the fully differentiated neurons during the progression of AD or other neurodegenerative diseases.
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Alzheimer's disease (AD), the most common neurodegenerative disease in the adult population, manifests the signs of cognitive decline, behavioral changes, and functional impairment. The underlying mechanisms for AD are not well-clarified yet, but the aggregation of amyloid-beta peptides (A beta s), the major components in the senile plaques observed in AD brains, contributes significantly to the disease progression. Emerging evidence reveals that aberrant cell cycle reentry may play a central role in A beta-induced neuronal demise. Recently, we have shown that several signaling mediators, including Id1, hypoxia-inducible factor-1 (HIF-1), cyclin-dependent kinases-5 (CDK5), and sonic hedgehog (Shh), may contribute to A beta-induced cell cycle reentry in postmitotic neurons; furthermore, Id1 and CDK5/p25 mutually antagonize the expression/activity of each other. Therefore, Id proteins may potentially have clinical applications in AD. In this review article, we introduce the underlying mechanisms for cell cycle dysregulation in AD and present some examples, including our own studies, to show different aspects of Id1 in terms of cell cycle reentry and other signaling that may be crucial to alter the neuronal fates in this devastating neurodegenerative disease. 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Biomedicine</subject><subject>Mammalian cells</subject><subject>Mammals</subject><subject>Models, Biological</subject><subject>Nervous system</subject><subject>Neuroblastoma</subject><subject>Neurodegenerative diseases</subject><subject>Neurogenesis</subject><subject>Neurons</subject><subject>Neurotoxicity</subject><subject>Peptides</subject><subject>Proteins</subject><subject>Review</subject><subject>Science &amp; Technology</subject><subject>Senescence</subject><subject>Senile plaques</subject><subject>Signal transduction</subject><subject>Stem cells</subject><subject>Therapeutic applications</subject><subject>Transcription factors</subject><issn>2073-4409</issn><issn>2073-4409</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNks1rFDEYxgdRbKm9eZaABwUdTSaZTeJBqGPVhYJQ9Bzy8c5ultmkJjPK-teb6dZl68lc8vV7H96Pp6qeEvyGUonfWhiGLDEnnC0eVKcN5rRmDMuHR-eT6jznDS5LkAXB7ePqhDYcC0roadVfbiGtfFih6zhARrFHy7D2xo8xzZePvu8hQRi9Hn0MNUE-oIvh9xp8CXyRC5BBZ3iHupIK6nZ2AHQNJSDtkA4OfYBdDO5J9ajXQ4bzu_2s-v7p8lv3pb76-nnZXVzVlnEx1gZT6SRfSA7SSmBCYkM57RtqCOUYHOdOUAGStG1vGWbGFhRAGgdWEE7PquVe10W9UTfJb3Xaqai9un2IaaV0Gn1JUhVx3jZa46LGpGtMy5gThAptWkrZrPV-r3UzmS04O9ekh3ui93-CX6tV_Kl4aTppSBF4eSeQ4o8J8qi2Ps8T0wHilFXDGt7IlmJa0Of_oJs4pVBaNVMLKbEUrFCv95RNMecE_SEZgtXsB3Xsh4I_Oy7gAP-dfgFe7YFfYGKfrYdg4YAVw7RtSZCw2TtzOeL_6c6Pt4bp4hRG-geXPdBQ</recordid><startdate>20200721</startdate><enddate>20200721</enddate><creator>Chen, Shang-Der</creator><creator>Yang, Jenq-Lin</creator><creator>Lin, Yi-Chun</creator><creator>Chao, A-Ching</creator><creator>Yang, Ding</creator><general>Mdpi</general><general>MDPI AG</general><general>MDPI</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1230-9622</orcidid><orcidid>https://orcid.org/0000-0002-9897-8087</orcidid><orcidid>https://orcid.org/0000-0001-5544-7561</orcidid><orcidid>https://orcid.org/0000-0001-7879-2579</orcidid></search><sort><creationdate>20200721</creationdate><title>Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer's Disease: Cell Cycle Reentry and Beyond</title><author>Chen, Shang-Der ; Yang, Jenq-Lin ; Lin, Yi-Chun ; Chao, A-Ching ; Yang, Ding</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-b039d97697e9c9e4890b373f23b1370ed77d838e9155fc404bc97eee9bdec8173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell adhesion &amp; migration</topic><topic>Cell Biology</topic><topic>Cell Cycle</topic><topic>cell cycle reentry</topic><topic>Cell Death</topic><topic>Cell differentiation</topic><topic>Cell migration</topic><topic>Cognitive ability</topic><topic>Cyclin-dependent kinase 5</topic><topic>Cyclin-dependent kinases</topic><topic>Deoxyribonucleic acid</topic><topic>Disease</topic><topic>DNA</topic><topic>Gene expression</topic><topic>Hedgehog protein</topic><topic>Helix-loop-helix proteins</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factor 1</topic><topic>Id1 protein</topic><topic>Inhibitor of Differentiation Protein 1 - metabolism</topic><topic>inhibitor of DNA-binding/differentiation proteins</topic><topic>Kinases</topic><topic>Life Sciences &amp; 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subjects Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Alzheimer's disease
Angiogenesis
Animals
Apoptosis
Cell adhesion & migration
Cell Biology
Cell Cycle
cell cycle reentry
Cell Death
Cell differentiation
Cell migration
Cognitive ability
Cyclin-dependent kinase 5
Cyclin-dependent kinases
Deoxyribonucleic acid
Disease
DNA
Gene expression
Hedgehog protein
Helix-loop-helix proteins
Humans
Hypoxia
Hypoxia-inducible factor 1
Id1 protein
Inhibitor of Differentiation Protein 1 - metabolism
inhibitor of DNA-binding/differentiation proteins
Kinases
Life Sciences & Biomedicine
Mammalian cells
Mammals
Models, Biological
Nervous system
Neuroblastoma
Neurodegenerative diseases
Neurogenesis
Neurons
Neurotoxicity
Peptides
Proteins
Review
Science & Technology
Senescence
Senile plaques
Signal transduction
Stem cells
Therapeutic applications
Transcription factors
title Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer's Disease: Cell Cycle Reentry and Beyond
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