Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD
Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dem...
Gespeichert in:
Veröffentlicht in: | The Neuroscientist 2024-04, Vol.30 (2), p.214-228 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 228 |
---|---|
container_issue | 2 |
container_start_page | 214 |
container_title | The Neuroscientist |
container_volume | 30 |
creator | Rayner, Stephanie L. Hogan, Alison Davidson, Jennilee M. Cheng, Flora Luu, Luan Morsch, Marco Blair, Ian Chung, Roger Lee, Albert |
description | Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dementia (FTD). Identifying gene mutations that cause ALS/FTD has provided valuable insight into the disease process. Several ALS/FTD-causing mutations occur within proteins with roles in protein clearance systems. This includes ALS/FTD mutations in CCNF, which encodes the protein cyclin F: a component of a multiprotein E3 ubiquitin ligase that mediates the ubiquitylation of substrates for their timely degradation. In this review, we provide an update on the link between ALS/FTD CCNF mutations and neurodegeneration. |
doi_str_mv | 10.1177/10738584221120182 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2709916973</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_10738584221120182</sage_id><sourcerecordid>2709916973</sourcerecordid><originalsourceid>FETCH-LOGICAL-c340t-457ad7a81035df396d290022a321860df51ec8ebbfb06d5051870941899e3f5f3</originalsourceid><addsrcrecordid>eNp9kMFKw0AQhhdRbK0-gBfJ0UNTZ3aT7C54KdWqUFSwnsMmu9umpNmaTQ59exNavQieZmC-_4f5CLlGmCByfofAmYhFRCkiBRT0hAwRhAwjkOK03zkLe2BALrzfQIdAxM_JgCWQUIYwJPezfV4WVTAfB6-mrZ02K1OZWjWFq8aBqnTQrE3wrpq16w--8IGzwXTxcTdfPlySM6tKb66Oc0Q-54_L2XO4eHt6mU0XYc4iaMIo5kpzJRBYrC2TiaYSgFLFKIoEtI3R5MJkmc0g0THEKDjICIWUhtnYshG5PfTuavfVGt-k28LnpixVZVzrU9rhEhPJWYfiAc1r531tbLqri62q9ylC2ktL_0jrMjfH-jbbGv2b-LHUAZMD4NXKpBvX1lX37j-N309wcJ8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2709916973</pqid></control><display><type>article</type><title>Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD</title><source>MEDLINE</source><source>SAGE Complete A-Z List</source><creator>Rayner, Stephanie L. ; Hogan, Alison ; Davidson, Jennilee M. ; Cheng, Flora ; Luu, Luan ; Morsch, Marco ; Blair, Ian ; Chung, Roger ; Lee, Albert</creator><creatorcontrib>Rayner, Stephanie L. ; Hogan, Alison ; Davidson, Jennilee M. ; Cheng, Flora ; Luu, Luan ; Morsch, Marco ; Blair, Ian ; Chung, Roger ; Lee, Albert</creatorcontrib><description>Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dementia (FTD). Identifying gene mutations that cause ALS/FTD has provided valuable insight into the disease process. Several ALS/FTD-causing mutations occur within proteins with roles in protein clearance systems. This includes ALS/FTD mutations in CCNF, which encodes the protein cyclin F: a component of a multiprotein E3 ubiquitin ligase that mediates the ubiquitylation of substrates for their timely degradation. In this review, we provide an update on the link between ALS/FTD CCNF mutations and neurodegeneration.</description><identifier>ISSN: 1073-8584</identifier><identifier>EISSN: 1089-4098</identifier><identifier>DOI: 10.1177/10738584221120182</identifier><identifier>PMID: 36062310</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - metabolism ; Cyclins - genetics ; Cyclins - metabolism ; Frontotemporal Dementia - genetics ; Frontotemporal Dementia - metabolism ; Humans ; Motor Neurons - metabolism ; Mutation</subject><ispartof>The Neuroscientist, 2024-04, Vol.30 (2), p.214-228</ispartof><rights>The Author(s) 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-457ad7a81035df396d290022a321860df51ec8ebbfb06d5051870941899e3f5f3</citedby><cites>FETCH-LOGICAL-c340t-457ad7a81035df396d290022a321860df51ec8ebbfb06d5051870941899e3f5f3</cites><orcidid>0000-0003-1590-0071 ; 0000-0001-5156-0567</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/10738584221120182$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/10738584221120182$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>313,314,778,782,790,21802,27905,27907,27908,43604,43605</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36062310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rayner, Stephanie L.</creatorcontrib><creatorcontrib>Hogan, Alison</creatorcontrib><creatorcontrib>Davidson, Jennilee M.</creatorcontrib><creatorcontrib>Cheng, Flora</creatorcontrib><creatorcontrib>Luu, Luan</creatorcontrib><creatorcontrib>Morsch, Marco</creatorcontrib><creatorcontrib>Blair, Ian</creatorcontrib><creatorcontrib>Chung, Roger</creatorcontrib><creatorcontrib>Lee, Albert</creatorcontrib><title>Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD</title><title>The Neuroscientist</title><addtitle>Neuroscientist</addtitle><description>Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dementia (FTD). Identifying gene mutations that cause ALS/FTD has provided valuable insight into the disease process. Several ALS/FTD-causing mutations occur within proteins with roles in protein clearance systems. This includes ALS/FTD mutations in CCNF, which encodes the protein cyclin F: a component of a multiprotein E3 ubiquitin ligase that mediates the ubiquitylation of substrates for their timely degradation. In this review, we provide an update on the link between ALS/FTD CCNF mutations and neurodegeneration.</description><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Cyclins - genetics</subject><subject>Cyclins - metabolism</subject><subject>Frontotemporal Dementia - genetics</subject><subject>Frontotemporal Dementia - metabolism</subject><subject>Humans</subject><subject>Motor Neurons - metabolism</subject><subject>Mutation</subject><issn>1073-8584</issn><issn>1089-4098</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFKw0AQhhdRbK0-gBfJ0UNTZ3aT7C54KdWqUFSwnsMmu9umpNmaTQ59exNavQieZmC-_4f5CLlGmCByfofAmYhFRCkiBRT0hAwRhAwjkOK03zkLe2BALrzfQIdAxM_JgCWQUIYwJPezfV4WVTAfB6-mrZ02K1OZWjWFq8aBqnTQrE3wrpq16w--8IGzwXTxcTdfPlySM6tKb66Oc0Q-54_L2XO4eHt6mU0XYc4iaMIo5kpzJRBYrC2TiaYSgFLFKIoEtI3R5MJkmc0g0THEKDjICIWUhtnYshG5PfTuavfVGt-k28LnpixVZVzrU9rhEhPJWYfiAc1r531tbLqri62q9ylC2ktL_0jrMjfH-jbbGv2b-LHUAZMD4NXKpBvX1lX37j-N309wcJ8</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Rayner, Stephanie L.</creator><creator>Hogan, Alison</creator><creator>Davidson, Jennilee M.</creator><creator>Cheng, Flora</creator><creator>Luu, Luan</creator><creator>Morsch, Marco</creator><creator>Blair, Ian</creator><creator>Chung, Roger</creator><creator>Lee, Albert</creator><general>SAGE Publications</general><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>7X8</scope><orcidid>https://orcid.org/0000-0003-1590-0071</orcidid><orcidid>https://orcid.org/0000-0001-5156-0567</orcidid></search><sort><creationdate>202404</creationdate><title>Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD</title><author>Rayner, Stephanie L. ; Hogan, Alison ; Davidson, Jennilee M. ; Cheng, Flora ; Luu, Luan ; Morsch, Marco ; Blair, Ian ; Chung, Roger ; Lee, Albert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-457ad7a81035df396d290022a321860df51ec8ebbfb06d5051870941899e3f5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Cyclins - genetics</topic><topic>Cyclins - metabolism</topic><topic>Frontotemporal Dementia - genetics</topic><topic>Frontotemporal Dementia - metabolism</topic><topic>Humans</topic><topic>Motor Neurons - metabolism</topic><topic>Mutation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rayner, Stephanie L.</creatorcontrib><creatorcontrib>Hogan, Alison</creatorcontrib><creatorcontrib>Davidson, Jennilee M.</creatorcontrib><creatorcontrib>Cheng, Flora</creatorcontrib><creatorcontrib>Luu, Luan</creatorcontrib><creatorcontrib>Morsch, Marco</creatorcontrib><creatorcontrib>Blair, Ian</creatorcontrib><creatorcontrib>Chung, Roger</creatorcontrib><creatorcontrib>Lee, Albert</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Neuroscientist</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rayner, Stephanie L.</au><au>Hogan, Alison</au><au>Davidson, Jennilee M.</au><au>Cheng, Flora</au><au>Luu, Luan</au><au>Morsch, Marco</au><au>Blair, Ian</au><au>Chung, Roger</au><au>Lee, Albert</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD</atitle><jtitle>The Neuroscientist</jtitle><addtitle>Neuroscientist</addtitle><date>2024-04</date><risdate>2024</risdate><volume>30</volume><issue>2</issue><spage>214</spage><epage>228</epage><pages>214-228</pages><issn>1073-8584</issn><eissn>1089-4098</eissn><abstract>Amyotrophic lateral sclerosis (ALS) is the most common form of motor neuron disease and is characterized by the degeneration of upper and lower motor neurons of the brain and spinal cord. ALS is also linked clinically, genetically, and pathologically to a form of dementia known as frontotemporal dementia (FTD). Identifying gene mutations that cause ALS/FTD has provided valuable insight into the disease process. Several ALS/FTD-causing mutations occur within proteins with roles in protein clearance systems. This includes ALS/FTD mutations in CCNF, which encodes the protein cyclin F: a component of a multiprotein E3 ubiquitin ligase that mediates the ubiquitylation of substrates for their timely degradation. In this review, we provide an update on the link between ALS/FTD CCNF mutations and neurodegeneration.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>36062310</pmid><doi>10.1177/10738584221120182</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-1590-0071</orcidid><orcidid>https://orcid.org/0000-0001-5156-0567</orcidid></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1073-8584 |
ispartof | The Neuroscientist, 2024-04, Vol.30 (2), p.214-228 |
issn | 1073-8584 1089-4098 |
language | eng |
recordid | cdi_proquest_miscellaneous_2709916973 |
source | MEDLINE; SAGE Complete A-Z List |
subjects | Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Cyclins - genetics Cyclins - metabolism Frontotemporal Dementia - genetics Frontotemporal Dementia - metabolism Humans Motor Neurons - metabolism Mutation |
title | Cyclin F, Neurodegeneration, and the Pathogenesis of ALS/FTD |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T17%3A49%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cyclin%20F,%20Neurodegeneration,%20and%20the%20Pathogenesis%20of%20ALS/FTD&rft.jtitle=The%20Neuroscientist&rft.au=Rayner,%20Stephanie%20L.&rft.date=2024-04&rft.volume=30&rft.issue=2&rft.spage=214&rft.epage=228&rft.pages=214-228&rft.issn=1073-8584&rft.eissn=1089-4098&rft_id=info:doi/10.1177/10738584221120182&rft_dat=%3Cproquest_cross%3E2709916973%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2709916973&rft_id=info:pmid/36062310&rft_sage_id=10.1177_10738584221120182&rfr_iscdi=true |