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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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. 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.</description><identifier>ISSN: 2073-4409</identifier><identifier>EISSN: 2073-4409</identifier><identifier>DOI: 10.3390/cells9071746</identifier><identifier>PMID: 32708313</identifier><language>eng</language><publisher>BASEL: Mdpi</publisher><subject>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</subject><ispartof>Cells (Basel, Switzerland), 2020-07, Vol.9 (7), p.1746, Article 1746</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>16</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000557291400001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c478t-b039d97697e9c9e4890b373f23b1370ed77d838e9155fc404bc97eee9bdec8173</citedby><cites>FETCH-LOGICAL-c478t-b039d97697e9c9e4890b373f23b1370ed77d838e9155fc404bc97eee9bdec8173</cites><orcidid>0000-0003-1230-9622 ; 0000-0002-9897-8087 ; 0000-0001-5544-7561 ; 0000-0001-7879-2579</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7409121/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7409121/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27929,27930,28253,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32708313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Shang-Der</creatorcontrib><creatorcontrib>Yang, Jenq-Lin</creatorcontrib><creatorcontrib>Lin, Yi-Chun</creatorcontrib><creatorcontrib>Chao, A-Ching</creatorcontrib><creatorcontrib>Yang, Ding</creatorcontrib><title>Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer's Disease: Cell Cycle Reentry and Beyond</title><title>Cells (Basel, Switzerland)</title><addtitle>CELLS-BASEL</addtitle><addtitle>Cells</addtitle><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.</description><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell Cycle</subject><subject>cell cycle reentry</subject><subject>Cell Death</subject><subject>Cell differentiation</subject><subject>Cell migration</subject><subject>Cognitive ability</subject><subject>Cyclin-dependent kinase 5</subject><subject>Cyclin-dependent kinases</subject><subject>Deoxyribonucleic acid</subject><subject>Disease</subject><subject>DNA</subject><subject>Gene expression</subject><subject>Hedgehog protein</subject><subject>Helix-loop-helix proteins</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factor 1</subject><subject>Id1 protein</subject><subject>Inhibitor of Differentiation Protein 1 - metabolism</subject><subject>inhibitor of DNA-binding/differentiation proteins</subject><subject>Kinases</subject><subject>Life Sciences & 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 & 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 & 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 & Biomedicine</topic><topic>Mammalian cells</topic><topic>Mammals</topic><topic>Models, Biological</topic><topic>Nervous system</topic><topic>Neuroblastoma</topic><topic>Neurodegenerative diseases</topic><topic>Neurogenesis</topic><topic>Neurons</topic><topic>Neurotoxicity</topic><topic>Peptides</topic><topic>Proteins</topic><topic>Review</topic><topic>Science & Technology</topic><topic>Senescence</topic><topic>Senile plaques</topic><topic>Signal transduction</topic><topic>Stem cells</topic><topic>Therapeutic applications</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Shang-Der</creatorcontrib><creatorcontrib>Yang, Jenq-Lin</creatorcontrib><creatorcontrib>Lin, Yi-Chun</creatorcontrib><creatorcontrib>Chao, A-Ching</creatorcontrib><creatorcontrib>Yang, Ding</creatorcontrib><collection>Web of Science - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cells (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Shang-Der</au><au>Yang, Jenq-Lin</au><au>Lin, Yi-Chun</au><au>Chao, A-Ching</au><au>Yang, Ding</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Emerging Roles of Inhibitor of Differentiation-1 in Alzheimer's Disease: Cell Cycle Reentry and Beyond</atitle><jtitle>Cells (Basel, Switzerland)</jtitle><stitle>CELLS-BASEL</stitle><addtitle>Cells</addtitle><date>2020-07-21</date><risdate>2020</risdate><volume>9</volume><issue>7</issue><spage>1746</spage><pages>1746-</pages><artnum>1746</artnum><issn>2073-4409</issn><eissn>2073-4409</eissn><abstract>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.</abstract><cop>BASEL</cop><pub>Mdpi</pub><pmid>32708313</pmid><doi>10.3390/cells9071746</doi><tpages>15</tpages><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><oa>free_for_read</oa></addata></record> |
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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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